2003: "Although the levels were low, subjects generally correctly
identified if they were truly dosed or not. Their task was to drive through
city streets while responding to traffic controls, crossing intersections
and making turns at intersections. Using driving instructors' performance
scores, Lamers and Ramaekers found essentially no differences between the
dosed and non-dosed conditions. However, they also found that drivers under
the THC-only condition evaluated their performance as significantly worse
than under the placebo, the alcohol and the alcohol+THC
condition. Thus, the study confirmed the hypothesis that, unlike alcohol,
marijuana actually enhances rather than mitigates the perception of impairment.
The only negative behavioral effect of THC was a slight reduction in the
frequency of intersections searched for cross traffic (based on the drivers'
eye movement records). Although statistically significant, the drop was
negligible: from a mean frequency of 85% of the intersections in the placebo
condition, to a mean frequency of 82% in the combined alcohol+THC condition."
 "CANNABIS",
State
of Knowledge of Drug-Impaired Driving, US
National
Highway Traffic Safety Administration (DOT HS 809 642), Sept 2003.

2002: "When Doctor Yesavage was funded by the federal government to
repeat the study with the simple controls that others and I [Dr
John P Morgan] had suggested,
they were unable to show any impact of marijuana use after four hours in
a similar group of people. Therefore, I believe that the truth is that marijuana
use will impact airplane and driving simulators and to some degree driving
performance for three hours to four hours after use; however there is no
sustained impact. Any impact is relatively minor. ... The study findings
show that cannabis alone does not increase the likelihood of responsibility
in an accident. However, most of the studies used a measurement of THC-COOH,
an inactive metabolite that can remain in urine for several days. When the
authors separated out THC alone, the risk ratio was slightly higher, even
though it did not reach the required level of significance. In addition,
as the concentration of THC increases, the more the ratio increases, once
again suggesting a dose-response relationship. Furthermore, the cannabis
and alcohol combination significantly increases risk.
Without being able to draw any definite conclusions, there are some signs
that their effects are in synergy and not merely additive. Studies on injured
drivers (Terhune (1982) and Hunter
(1998)) have ratios somewhat higher than in the other studies on fatal accidents.
According to Bates and Blakely (1999), the apparent reduction in the risk
of a fatal accident stems from the fact that drivers under the influence
of cannabis drive less dangerously, for example by reducing their speed."

"Cannabis:
Our Position for a Canadian Public Policy", Report of the Senate Special
Committee on Illegal Drugs, Vol 1, Chapter 8, Sept 2002.

2000: "In conclusion, cannabis impairs driving behaviour. However,
this impairment is mediated in that subjects under cannabis treatment appear
to perceive that they are indeed impaired. Where they can compensate, they
do, for example, by not overtaking, by slowing down and by focusing their
attention when they know a response will be required. However, such compensation
is not possible where events are unexpected or where continuous attention
is required. Effects of driving behaviour are present up to an hour after
smoking but do not continue for extended periods." 
"Cannabis and driving:
a review of the literature and commentary (No 12)", Chapter 11, Department
of Transport, United Kingdom
Government

2000: "... [United Kingdom] government-funded research ... shows that
driving under the influence of drugs makes motorists more cautious and has
a limited impact on their risk of crashing. In the study, conducted by the
Transport Research Laboratory, grade A cannabis specially imported from America
was given to 15 regular users. ... drivers were then put through four weeks
of tests on driving simulators to gauge reaction times and awareness. Regular
smokers were used because previous tests in America using first-timers resulted
in the volunteers falling over and feeling ill. The laboratory found its
guinea pigs through what it described as a 'snowballing technique' - one
known user was asked to find another after being promised anonymity and exemption
from prosecution agreed with the Home Office. Instead of proving that drug-taking
while driving increased the risk of accidents, researchers found that the
mellowing effects of cannabis made drivers more cautious and so less likely
to drive dangerously. Although the cannabis affected reaction time in regular
users, its effects appear to be substantially less dangerous than fatigue
or drinking. Research by the Australian Drugs Foundation found that cannabis
was the only drug tested that decreased the relative risk of having an accident.
The findings will embarrass ministers at the Department of the Environment,
Transport and the Regions (DETR) who commissioned the study after pressure
from motoring organisations and anti-drug campaigners. Lord Whitty, the transport
minister, will receive the report later this month. Last week police revealed
details of new drug-driving tests to be administered by the roadside, which
were received with some amusement. They require suspected drug-drivers to
stand on one leg, lean back and touch their nose with their eyes closed,
and to count to 30 silently with their eyes shut. This is apparently difficult
for those on a drug trip. ... if the findings are less than frightening on
the effects of marijuana, they may convince [UK] ministers to put more money
into raising driver awareness of fatigue. Tiredness is now blamed for causing
10% of all fatal accidents, compared with 6% for
alcohol and 3% for drugs. The report's surprising
conclusions will not sway organisations such as the RAC, which believes there
is incontrovertible evidence that drug-driving is a growing menace. DETR
statistics published in January showed a six-fold increase in the number
of people found to be driving with drugs in their system after fatal road
accidents. The figure jumped from 3% in 1989 to 18%. Dr Rob Tunbridge, the
report's author, refused to reveal his findings before they were published
but said: 'If you were to ask me to rank them in order of priority, fatigue
is the worst killer, followed by alcohol, and drugs follow way behind in
third.' Tunbridge admitted that the effect of drugs differed with the individual,
the amount taken, the environment they were taken in and the point at which
you tested reactions." claims Jonathan Carr-Brown from
"Cannabis may
make you a safer driver", Times United Kingdom, Aug 13 2000.

1999: "Recent research into impairment and traffic accident reports
from several countries shows that marijuana taken alone in moderate amounts
does not significantly increase a driver's risk of causing an accident --
unlike alcohol ... While smoking marijuana does impair
driving ability, it does not share alcohol's effect on judgment. Drivers
on marijuana remain aware of their impairment, prompting them to slow down
and drive more cautiously to compensate ..." claims Alison Smiley, University
of Toronto researcher, from
"Marijuana
Not a Factor in Driving Accidents", Mar 29 1999.

1998: "The largest study ever done linking road accidents with drugs
and alcohol has found drivers with cannabis in their
blood were no more at risk than those who were drug-free. In fact, the findings
by a pharmacology team from the University of Adelaide and Transport SA showed
drivers who had smoked marijuana were marginally less likely to have an accident
than those who were drug-free. ... the difference was not great enough to
be statistically significant but could be explained by anecdotal evidence
that marijuana smokers were more cautious and drove more slowly because of
altered time perception." claims Dr Jason White from
"Cannabis and driving",
Canberra Times, Oct 21 1998.

1996: "Compared to alcohol, which makes people
take more risks on the road, marijuana made drivers slow down and drive more
carefully.... Cannabis is good for driving skills, as people tend to
overcompensate for a perceived impairment." claims Professor Olaf Drummer,
forensic scientist, Royal College of Surgeons in Melbourne, Australia.

1994: "The study showed that a modest dose of
alcohol (BAC = 0.034 g%) produced a significant impairment
in city driving, as measured by the molar approach, relative to a placebo.
More specifically, alcohol impaired both vehicle handling and traffic maneuvers.
Marijuana, administered in a dose of 100Êµg/kg THC, on the other
hand, did not significantly change mean driving performance as measured by
this approach. ... The results of the studies corroborate those of previous
driving simulator and closed-course tests by indicating that THC in inhaled
doses up to 300 µg/kg has significant, yet not dramatic, dose-related
impairing effects on driving performance. Standard deviation of lateral position
in the road-tracking test was the most sensitive measure for revealing THC's
adverse effects. ... Evidence from the present and previous studies strongly
suggests that alcohol encourages risky driving whereas THC encourages greater
caution, at least in experiments. Another way THC seems to differ qualitatively
from many other drugs is that the former's users seem better able to compensate
for its adverse effects while driving under the influence." claims
Hindrik W J Robbe,
"Marijuana use and
driving",
Journal
of the International Hemp Association (defunct), vol 1, pgs 44-48

1993: "This program of research has shown that marijuana, when taken
alone, produces a moderate degree of driving impairment which is related
to the consumed THC dose. The impairment manifests itself mainly in the ability
to maintain a steady lateral position on the road, but its magnitude is not
exceptional in comparison with changes produced by many medicinal drugs and
alcohol. Drivers under the influence of marijuana
retain insight in their performance and will compensate, where they can,
for example, by slowing down or increasing effort. As a consequence, THC's
adverse effects on driving performance appear relatively small. THC's effects
on road-tracking after doses up to 300 g/kg never exceeded alcohol's at bacs
of 0.08 %; and, were in no way unusual compared to many medicinal drugs'
(Robbe, 1994; Robbe and O'Hanlon, 1995; O'Hanlon et al., 1995). Yet, THC's
effects differ qualitatively from many other drugs, especially alcohol. Evidence
from the present and previous studies strongly suggests that alcohol encourages
risky driving whereas THC encourages greater caution, at least in experiments.
Another way THC seems to differ qualitatively from many other drugs is that
the former's users seem better able to compensate for its adverse effects
while driving under the influence. Although THC's adverse effects on driving
performance appeared relatively small in the tests employed in this program,
one can still easily imagine situations where the influence of marijuana
smoking might have a dangerous effect; i.e., emergency situations which put
high demands on the driver's information processing capacity, prolonged
monotonous driving, and after THC has been taken with other drugs, especially
alcohol. Because these possibilities are real, the results of the present
studies should not be considered as the final word. They should, however,
serve as the point of departure for subsequent studies that will ultimately
complete the picture of THC's effects on driving performance." claims
"Marijuana
and Actual Driving Performance" (DOT HS 808 078, Final Report, Nov 1993),
US National
Highway Traffic Safety Administration

1987: In January, 16 persons die and 170 are injured after an engineer
drunk on alcohol passes out and crashes his Amtrak
passenger train into three locomotives. The engineer had also been smoking
cannabis. Many cannabis prohibitionists point to this incident when arguing
that cannabis use is not a victimless act.

Cannabis and Road Safety, research studies to examine the effects
of cannabis on driving skills and on actual driving performance by Dr.
G.B.Chesher, Department of Pharmacology University of Sydney and National
Drug and Alcohol Research Centre University of New South Wales, Australia.shug.co.uk/research/driving2.htm

Acquired Immune Deficiency Syndrome

2005: "Controlled studies have revealed therapeutic utility of
cannabinoids in the treatment of ... AIDS wasting syndrome ... THC itself
is approved in the U.S. by the FDA, and it is used in many other countries
... for appetite enhancement. We, and many others, have found that not only
THC does that, but also the endocannabinoids. This is one of the main reasons
for high endocannabinoid levels during hunger and so on. Now, THC can be
used, and is being used, for these two things." claims Dr
Raphael Mechoulam, as reported
by David Jay Brown,
"The
New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael
Mechoulam".

2000: "A study by researchers from the University of California, San
Francisco has found that patients with HIV infection taking protease inhibitors
do not experience short-term adverse virologic effects from using cannabinoids.
... All three groups gained weight. Part of that was due to regularly scheduled
meals and snacks being readily available. However, the placebo arm averaged
a gain of 1.30 kilograms while the subjects who took oral dronabinol gained
an average of 3.18 kilograms. Those who smoked marijuana gained an average
of 3.51 kilograms. Caloric intake reflected the same order." claims Dr
Donald I Abrams from
"Marijuana
does not appear to alter viral loads of hiv patients taking protease
inhibitors", July 13 2000.

1997: Australian AIDS patients who use cannabis have a better quality
of life and patients with AIDS for more than 10 years find cannabis to be
critical. One patient believes cannabis to be his "savior", claims
"Dope
Use Improves Lives of Patients: Research", Canberra Times, Jan
15 1997.

2004: "Short-term cannabis use does not seem to adversely affect CD4+
cell counts or viral loads in HIV -infected patients, according to a report
published in the August 19th issue of the Annals of Internal Medicine.
In HIV-infected patients, marijuana has been used as an appetite stimulant
and as a treatment for the nausea associated with some antiretroviral agents.
However, concern has been raised that such therapy could have a harmful effect
on disease status, because in theory, cannabinoid use could increase HIV
levels by impairing the immune response or by interfering with the activity
of protease inhibitors. Previously it was shown that short-term marijuana
use did not influence nelfinavir metabolism. Although marijuana use did produce
a drop in indinavir levels, this fall was small and unlikely to be clinically
meaningful. However, it still remained unclear whether cannabinoid use had
an effect on viral load or CD+ cell counts. To investigate, Dr.
Donald I. Abrams, from the University
of California at San Francisco, and colleagues assessed the outcomes of 67
HIV-infected patients who were randomly assigned to use marijuana cigarettes,
cannabinoid capsules, or sugar pills (placebo) three times daily for 21 days.
All of the patients had been receiving the same antiretroviral regimen, which
included indinavir or nelfinavir, for at least 8 weeks before the study began.
More than half of the subjects in each group had undetectable viral loads
throughout the study, the researchers note. Although not statistically
significant, marijuana and cannabinoid use were actually associated with
a slight drop in viral load compared with placebo use. Marijuana and cannabinoid
use did not produce a drop in CD4+ or CD8+ cell counts. In fact, compared
with placebo use, treatment with these agents was actually associated with
a slight increase in cell counts. The results suggest that short-term cannabinoid
use is not unsafe for patients with HIV infection, the authors note. 'Further
studies investigating the therapeutic potential of marijuana and other
cannabinoids in patients with HIV infection and other populations are ongoing
and should provide additional safety information over longer exposure periods,'
they write." 
"Marijuana
use does not accelerate HIV infection", PakTribune & 420 Magazine,
Dec 27 2004

2000: "A study by researchers from the University of California, San
Francisco has found that patients with HIV infection taking protease inhibitors
do not experience short-term adverse virologic effects from using cannabinoids.
... All three groups gained weight. Part of that was due to regularly scheduled
meals and snacks being readily available. However, the placebo arm averaged
a gain of 1.30 kilograms while the subjects who took oral dronabinol gained
an average of 3.18 kilograms. Those who smoked marijuana gained an average
of 3.51 kilograms. Caloric intake reflected the same order." claims Dr
Donald I Abrams from
"Marijuana
does not appear to alter viral loads of hiv patients taking protease
inhibitors", July 13 2000.

"Studies on certain species of rats using high doses of THC showed observable
suppression of the immune system and the actions of 'tumoricidal' cells.
This evidence suggests that the wonderful auto-immune-disease-curative powers
of THC measured in 1989 ... has a negative side to it - perhaps THC allows
cancer and opportunistic infections to spread more easily? A report by the
National Toxicology Program failed to support this notion. As described in
AIDS Treatment News, the research project tested rats for two years
with a steady dose of either THC or placebo. The THC dose was extremely high.
The rats on THC lived longer and developed fewer tumors than those on the
placebo. This report was not released on schedule and people have suggested
it was deliberately suppressed because the results were too shocking." claims
Los Angeles Cannabis Resource Center from "Cannabinoids in the Immune System".

Addiction

2006: "Now, marijuana's addictiveness is supported by clinical and
epidemiological studies based on the American Psychiatric Association's
diagnostic manual. But marijuana for some time has been widely used as a
countercultural recreational drug, and drug policy reformers in particular
refuse to apply the addictive label to this substance. Political conservatives,
on the other hand, insist on the harmfulness of marijuana as a tenet of their
drug policy. The grounds are thus set for perpetual conflict around the drug,
conflict that cannot be resolved by clinical designations or epidemiological
research. ... The addictiveness of caffeine, for example in coffee, is
periodically rediscovered (see Juliano & Griffiths, 2004), but ignored
because people mainly don't care about addiction to this popular, legal,
accepted drug (unless, occasionally, someone is trying to quit). Moreover,
caffeine dependence is not considered in the American Psychiatric Association's
diagnostic manual, DSM-IV ... In recent years, however, middle-class whites
have discovered that marijuana is a relatively safe experience. Although
we still get sporadic, alarmist reports on one or another harmful aspect
of marijuana, respected organs of society are now calling for the
decriminalization of the drug. We are near the end of a process of cultural
acceptance of marijuana. Students and young professionals, many of whom lead
very staid lives, have become comfortable with it, while still feeling sure
that people who take heroin become addicted. ... The two most widely
used substances that are thought of as addictive are cigarettes and alcohol.
These are legal, and there is no serious effort in place to proscribe them.
These are joined by pain killers, which are also widely recognized as addictive
(such as, most recently, Oxycontin; Peele, 2004). Obviously, we are prepared
to accept addictive drugs in our legal pharmacopoeia. ... What is the correct
attitude towards marijuana's addictive potential? We need to recognize that
addiction is not so much bound up in the characteristics of drugs (aside
from their ability to modify mood quickly and predictably), as it is in the
situations of users. ... But a spate of recent studies have identified a
marijuana dependence syndrome in about 10 percent of current users. ... For
the most part, the debate over marijuana's addictiveness is all flash and
no substance. Certainly, marijuana is addictive - as are coffee, antidepressants,
and tranquilizers. This, in itself, has no weight in policy decisions about
marijuana." claims internationally recognized addiction expert
Stanton Peele from
"Marijuana Is Addictive
- So What?", Jan 18 2006.

2004: "All patients reported benefit, indicating that for at
least a subset of alcoholics, cannabis use is associated with reduced drinking.
... There are ample references, however, to the use of cannabis as
a substitute for opiates (Birch 1889) and
as a treatment for delirium tremens (Clendinning 1843; Moreau 1845), which
were among the first uses by European physicians. ... At the turn of the
19th century in the United States, cannabis was listed as a treatment for
delirium tremens in standard medical texts (Edes 1887; Potter 1895) and manuals
(Lilly 1898; Merck 1899; Parke Davis 1909). Since delirium tremens is associated
with advanced alcoholism, we can adduce that patients who were prescribed
cannabis and used it on a long term basis were making a successful substitution.
... The patient had observed that when she smoked marijuana socially on weekends
she decreased her alcoholic intake. She was instructed to substitute cannabis
any time she felt the urge to drink. This regimen helped her to reduce her
alcohol intake to zero. ... Even if use is daily,
cannabis replacing alcohol (or other addictive, toxic drugs) reduces harm
because of its relatively benign side-effect profile. Cannabis-only usage
is not associated with car crashes; it does not damage the liver, the esophagus,
the spleen or the digestive tract. The chronic alcohol-inebriation-withdrawal
cycle ceases with successful cannabis substitution. Sleep and appetite are
restored, ability to focus and concentrate is enhanced, energy and activity
levels are improved, and pain and muscle spasms are relieved. Family and
social relationships can be sustained as pursuit of long-term goals ends
the cycle of crisis and apology. ... Treating alcoholism by cannabis substitution
creates a different doctor-patient relationship. Patients seek out the physician
to confer legitimacy on what they are doing or are about to do. My most important
service is to end their criminal status, Aeschalapian protection from the
criminal justice system, which often brings an expression of relief. An alliance
is created that promotes candor and trust. The physician is permitted to
act as a coach or an enabler in a positive sense." claims
Tod Hiro Mikuriya from
"Cannabis as
a Substitute for Alcohol",
O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Summer 2003.

2001: "Cannabis has long been described as creating a unique dual
consciousness, its users simultaneously in and outside the "real world."
Contrast this to the world surrounding users of large amounts of alcohol.
For many of the patients in this study, the shift from alcohol to cannabis
opened a new option on what had been an intractable and worsening problem.
In using cannabis as a substitute for alcohol, the cumulated problems of
a hard alcoholic life did not disappear; but they could be seen and act upon
from a distance, and soberly. At minimum, more effective coping and control
resulted from cannabis substitution. Hope is restored with relief from chronic
poisoning, and a life line back to functionality and dreams replaces injuries
and nightmares." claim Tod Hiro
Mikuriya and Jerry Mandel from
"Cannabis
Substitution: Harm Reduction Treatment for Alcoholism and Drug Dependence",
by Oct 2001

1990: "To rank today's commonly used drugs by their addictiveness,
we asked experts to consider two questions: How easy is it to get hooked
on these substances and how hard is it to stop using them? Although a person's
vulnerability to drug also depends on individual traits  physiology,
psychology, and social and economic pressures  these rankings reflect
only the addictive potential inherent in the drug. The numbers below are
relative rankings, based on the experts' scores for each substance:"

2003: "Cannabis reduces likelihood of violence during intoxication,
but mounting evidence associates withdrawal with aggressivity. ... While
cannabis has historically been excoriated for being a social 'menace' and
for inducing homicidal rages (Julien, 1992), more contemporary research indicates
cannabis-intoxicated individuals are in fact less likely to act aggressively.
However, a developing literature demonstrates an authentic cannabis withdrawal
syndrome, one symptom of which may be increased likelihood of interpersonal
aggression. ... the effects of tetrahydrocannabinol (THC) (the primary
psychoactive component of cannabis) on aggressive behavior have been studied
at length, with the preponderance of studies focusing on the acute effects
of THC intoxication. The results of these studies suggest that while low
doses of THC may slightly increase aggression, moderate and high doses can
suppress or even eliminate aggressive behavior (Myerscough & Taylor,
1986; Taylor, 1976). ... The animal literature also largely fails to support
the cannabisviolence relationship; cannabis administration tends to
foster submissive behaviors and suppress attack behaviors (Miczek, 1978;
Sieber, Frischknect, & Waser, 1980). ... According to legislators, one
of the reasons drugs are made illegal and the cost of policing and legislating
justifiable is to curb the threat of violence. There are two ironies to this.
First, the drug we know to be most likely to induce aggressive behavior
[alcohol] is not only readily and legally available,
it is often sold by the state for profit. Second, the greatest amount of
drug-related violence may be due to the means of regulating an illegal and
highly profitable industry (Fagin & Chin, 1990)." claims Peter N S Hoakena,
Sherry H Stewart from
"Drugs
of abuse and the elicitation of human aggressive behavior", Addictive
Behaviors, vol 28, pgs 1533-1554.

Alcoholism

2003: "All patients reported benefit, indicating that for at least
a subset of alcoholics, cannabis use is associated with reduced drinking.
The cost of alcoholism to individual patients and society-at-large warrants
testing of the cannabis-substitution approach and study of the drug-of-choice
phenomenon. ... As could be expected among patients seeking physician approval
to treat alcoholism with cannabis, all reported that theyd found it
'very effective' (41) or 'effective' (38). Efficacy was inferred from other
responses on seven questionnaires. ... Nine patients reported that they practiced
total abstinence from alcohol and attributed their
success to cannabis. Their years in sobriety: 19, 18, 16, 10, 7, 6, 4 (2),
and 2. Twenty-nine patients reported a return of symptoms when cannabis was
discontinued. Typical comments: 'I quit using cannabis while I was in the
army and my drinking doubled. I was also involved in several violent incidents
due to alcohol.'  reports Dr Tod
Hiro Mikuriya, MD from
"Cannabis as
a Substitute for Alcohol",
O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Summer 2003.

Alzheimer's

2014: "Can pot combat Alzheimer’s disease? That’s the intriguing suggestion
by neuroscientists who have found that even very low doses of a compound found in
marijuana may slow or halt the progression of the condition.
The study, conducted by the University of South Florida, trace amounts of THC —
short for delta-9-tetrahydrocannabinol — block the accumulation of
amyloid beta proteins in the brain, which have been linked to the memory-robbing disease.
These low concentrations of THC also selectively enhanced cellular functions that
help supply energy, transmit signals, and maintain a healthy brain.
'THC is known to be a potent antioxidant with neuroprotective properties,
but this is the first report that the compound directly affects Alzheimer’s
pathology by decreasing amyloid beta levels, inhibiting its aggregation,
and enhancing mitochondrial function,' said lead researcher Chuanhai Cao,
a neuroscientist at the Byrd Alzheimer’s Institute and the USF College of Pharmacy."
from "Does Pot Fight Alzheimer's?"
by Nick Tate, Aug 28 2014

2005: "The active ingredient in marijuana may stall decline from
Alzheimer's disease, research suggests. Scientists showed a synthetic version
of the compound may reduce inflammation associated with Alzheimer's and thus
help to prevent mental decline. They hope the cannanbinoid may be used to
developed new drug therapies. The research, by Madrid's Complutense University
and the Cajal Institute, is published in the Journal of Neuroscience.
The scientists first compared the brain tissue of patients who died from
Alzheimer's disease with that of healthy people who had died at a similar
age. They looked closely at brain cell receptors to which cannabinoids bind,
allowing their effects to be felt. They also studied structures called microglia,
which activate the brain's immune response. Microglia collect near the plaque
deposits associated with Alzheimer's disease and, when active, cause
inflammation. The researchers found a dramatically reduced functioning of
cannabinoid receptors in diseased brain tissue. This was an indication that
patients had lost the capacity to experience cannabinoids' protective effects.
The next step was to test the effect of cannabinoids on rats injected with
the amyloid protein that forms Alzheimer's plaques. Those animals who were
also given a dose of a cannabinoid performed much better in tests of their
mental functioning. The researchers found that the presence of amyloid protein
in the rats' brains activated immune cells. However, rats that also received
the cannabinoid showed no sign of microglia activation. Using cell cultures,
the researchers confirmed that cannabinoids counteracted the activation of
microglia and thus reduced inflammation. ... Researcher Dr Maria de Ceballos
said: 'These findings that cannabinoids work both to prevent inflammation
and to protect the brain may set the stage for their use as a therapeutic
approach for Alzheimer's disease.' Dr Susanne Sorensen, head of research
at the Alzheimer's Society, said: 'This is important research because it
provides another piece of the jigsaw puzzle on the workings of the brain.
There is no cure for Alzheimer's disease, so the identification of another
target for drug development is extremely welcome. The Alzheimer's Society
looks forward to seeing further research being carried out on cannabinoid
receptors as drug targets for Alzheimer's disease but would warn the public
against taking marijuana as a way of preventing Alzheimer's. It is now generally
recognised that as well as providing a 'high', long-term use of marijuana
can also lead to depression in many individuals.' ... Harriet Millward, of
the Alzheimer's Research Trust, said there were two main types of cannabinoid
receptor, CR1 and CR2. 'It is CR1 that produces most of the effects of marijuana,
including the harmful ones. If it is possible to make drugs that act only
on CR2, as suggested by the authors of this study, they might mimic the positive
effects of cannabinoids without the damaging ones of marijuana. However,
this is a fairly new field of research and producing such selective drugs
is not an easy task. There is also no evidence yet that cannabinoid-based
drugs can slow the decline in human Alzheimer's patients." 
"Marijuana may block
Alzheimer's", BBC News, Feb 22 2005.

"Another very intriguing link between natural cannabinoids and memory was
found in the brains of people who died of Alzheimer's disease. The researchers
discovered that the brains of people died of Alzheimer's showed substantially
less cannabinoid binding than shown by the brains of the control group. The
abnormal absences of cannabinoid receptors weren't located in regions correleated
with the damage done by Alzhemier's disease itself, so the researchers did
not believe that the Alzheimer's disease caused the disappearance of CB1
receptors. The difference between the Alzheimer's and control CB1 levels
was the highest in the hippocampus, the same region of the brain where
cannabinoids help regulate short-term memory. The Alzheimer's brains showed
binding to the test cannabinoid that was reduced by 49% compared to the binding
observed in the control brains. There is not yet an explanation for this
difference. Research showed that in rats, cannabinoid receptors and the ability
to respond to anandamide (and THC) develop gradually from birth until adulthood,
and then remain fairly constant as the animals age." claims
Los Angeles Cannabis
Resource Center (defunct) from
"Cannabinoids in
the brain".

Amotivation

includes "amotivational syndrome", "pacifist syndrome"
also see Aggression

1978: "Federally funded studies of long-tern users of high-potency
marijuana in three foreign countries showed no difference between the health,
ability to work, and brain function of users and non-users, a number of
researchers said ... Dr Sidney Cohen of the University of California at Los
Angeles, former head of drug research at the National Institute of Mental
Health, added that studies of marijuana users at UCLA and University of
California at Berkeley disputed the notion that smoking pot killed a student's
motivation to work. But Dr Glen D Mellinger, in his studies of Berkeley students,
concluded that the dropouts were poorly motivated even before they began
using marijuana and the poor motivation may have led to drug use instead
of the other way around." reports Stuart Auerbach in "Studies See No Health
Effect of Pot Smoking, Researchers Say", Washington Post, Jan 28,
1978.

Amyotrophic Lateral Sclerosis

2004: "Cannabis (marijuana) has been proposed as treatment for a widening
spectrum of medical conditions and has many properties that may be applicable
to the management of amyotrophic lateral sclerosis (ALS). This study is the
first, anonymous survey of persons with ALS regarding the use of cannabis.
There were 131 respondents, 13 of whom reported using cannabis in the last
12 months. Although the small number of people with ALS that reported using
cannabis limits the interpretation of the survey findings, the results indicate
that cannabis may be moderately effective at reducing symptoms of appetite
loss, depression, pain, spasticity, and drooling. Cannabis was reported
ineffective in reducing difficulties with speech and swallowing, and sexual
dysfunction. The longest relief was reported for depression (approximately
two to three hours)." 
Abstract of "Survey
of cannabis use in patients with amyotrophic lateral sclerosis" by Dagmar
Amtmann, Patrick Weydt, Kurt L Johnson, Mark P Jensen,
Gregory T Carter,
American Journal of Hospice
& Palliative Medicine, Mar-Apr 2004, pgs 95-104.
norml.org/index.cfm?Group_ID=6012

"Marijuana is a substance with many properties that may be applicable to
the management of amyotrophic lateral sclerosis (ALS). These include analgesia,
muscle relaxation, bronchodilation, saliva reduction, appetite stimulation,
and sleep induction. In addition, marijuana has now been shown to have strong
antioxidative and neuroprotective effects, which may prolong neuronal cell
survival. In areas where it is legal to do so, marijuana should be considered
in the pharmacological management of ALS. Further investigation into the
usefulness of marijuana in this setting is warranted." claim
Gregory T Carter, MD and
Bill S Rosen, MD from
"Marijuana
In The Management of Amyotrophic Lateral Sclerosis"

Anorexia

Anxiety

2005: "We show that 1 month after chronic HU210 [a potent synthetic
cannabinoid] treatment, rats display increased newborn neurons in the hippocampal
dentate gyrus and significantly reduced measures of anxiety- and depression-like
behavior. Thus, cannabinoids appear to be the only illicit drug whose capacity
to produce increased hippocampal newborn neurons is positively correlated
with its anxiolytic- [anti-anxiety] and antidepressant-like effects. ...
To determine the relationship between hippocampal neurogenesis and anxiolytic-
and antidepressant-like effects produced by chronic HU210, we examined the
effects of a selective destruction of the hippocampal neural stem cells on
the behavioral effects of chronic HU210. During the course of receiving chronic
HU210 injections, 1 group of Long-Evans rats received two 5-Gy doses of x-rays
confined to a limited brain region including the hippocampus ... Because
two 5-Gy doses of x-rays were not found to alter the morphology and function
of mature neurons in the hippocampus, hypothalamus, and amygdala, our results
together suggest that chronic HU210 treatment reduced anxiety and depression,
likely via promoting hippocampal neurogenesis. It has been shown that acute,
high doses of CB1 agonists or cannabinoids produced anxiety-like effects
in ratsor depression-like effects in mice. We observed here that chronic
administration of high, but not low, doses of HU210 exerts anxiolytic- and
antidepressant-like effects. To make things more complicated, acute, low
doses of cannabinoids have been found to induce anxiolytic-like effects in
rodents. These complicated effects of high and low doses of acute and chronic
exposure to cannabinoids may explain the seemingly conflicting results observed
in clinical studies regarding the effects of cannabinoid on anxiety and
depression. In summary, since adult hippocampal neurogenesis is suppressed
following chronic administration of opiates,
alcohol, nicotine, and
cocaine, the present study suggests that cannabinoids
are the only illicit drug that can promote adult hippocampal neurogenesis
following chronic administration. Increased hippocampal neurogenesis appears
to underlie the mechanism of anxiolytic- and antidepressant-like effects
produced by a high dose of chronic HU210 treatment. The opposing effects
of high doses of acute and chronic cannabinoids, together with the
anxiolytic-like effects caused by a low dose of cannabinoids, may finally
explain discrepancies in the clinical study literature regarding the effects
of cannabinoid on anxiety and depression." claims Wen Jiang, Yun Zhang, Lan
Xiao, Jamie Van Cleemput, Shao-Ping Ji, Guang Bai, Xia Zhang,
"Cannabinoids
promote embryonic and adult hippocampus neurogenesis and produce anxiolytic-
and antidepressant-like effects",
Journal of Clinical Investigation,
Nov 1 2005. PDF

2002: "Brain chemicals similar to those in cannabis wipe out bad memories
- and could point to new drugs for severe anxiety. The chemicals are called
cannabinoids. Mice with faulty cannabinoids can't forget traumatic events,
Beat Lutz of the Max Planck Institute of Psychiatry in Munich, Germany and
his colleagues have found. They suggest that the chemicals wipe fearful memories
from the brain. Drugs that boost cannabinoids could help people who suffer
post-traumatic stress disorder, phobias and panic attacks, say the researchers.
Its 'a great new idea,' says neuroscientist Pankaj Sah of the Australian
National University in Canberra: 'It introduces a whole new target,' for
such therapies, he says." reports Helen Pearson from
"Innate
cannabis chemical erases fears: Calming brain circuit could treat
anxieties", Nature, Aug 1 2002.

Appetite

2005: "THC itself is approved in the U.S. by the FDA, and it is used
in many other countries for the prevention of vomiting during cancer
chemotherapy, and for appetite enhancement. We, and many others, have found
that not only THC does that, but also the endocannabinoids. This is one of
the main reasons for high endocannabinoid levels during hunger and so on.
Now, THC can be used, and is being used, for these two things. ...
Sanofi-Synthélabo Recherché in France is doing some interesting
work. They have a compound, which is an antagonist of the cannabinoid system,
and they have tested it in about eight thousand obese people. They have found
that it is extremely useful. Their appetite goes down slowly, as it should,
and they lose weight. They plan to introduce the compound in twelve months
time, I think. They're doing a lot of work in the field, and they expect
huge sales." claims Dr Raphael
Mechoulam, as reported by David Jay Brown,
"The
New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael
Mechoulam".

2000: "A study by researchers from the University of California, San
Francisco has found that patients with HIV infection taking protease inhibitors
do not experience short-term adverse virologic effects from using cannabinoids.
... All three groups gained weight. Part of that was due to regularly scheduled
meals and snacks being readily available. However, the placebo arm averaged
a gain of 1.30 kilograms while the subjects who took oral dronabinol gained
an average of 3.18 kilograms. Those who smoked marijuana gained an average
of 3.51 kilograms. Caloric intake reflected the same order." claims Dr
Donald I Abrams, Professor of Clinical
Medicine, University of California at San Francisco from
"Marijuana
Does Not Appear To Alter Viral Loads of HIV Patients Taking Protease
Inhibitors", July 13 2000.
also at
cannabismd.org/reports/abrams1.php,
marijuananews.com/news.php3?sid=253

1986: "I started feeling the changes pretty much right away. Smoking
marijuana also felt ten times better than taking Marinol
pill. It helped reduce my nausea and I could hold down
food better." claims Jim Kerns, cancer
and chemotherapy patient.

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ...
My neurologist prescribed the drugs Compazine and Antivert. They had little
affect on the nausea and no affect on the appetite, even after the dosage
was doubled. After a couple of weeks of feeling sick and not eating, I had
lost 15 pounds and no medication was helping. ... I decided to try smoking
Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke
were gone I began to relax and get an appetite. I could finally eat again.
Since that time, I have used cannabis to maintain a healthy body weight and
a decent standard of living. For years I left my prescription drugs setting
on the counter, as Cannabis was more effective." claims John E Precup from
"Patient
Testimonials"

Arthritis

2005: "Controlled studies have revealed therapeutic utility of
cannabinoids in the treatment of ... rheumatoid arthritis ... many years
ago we elucidated the structure of a compound called
cannabidiol, which is present in very large amounts
in cannabis. It's more than THC, and it is anti-inflammatory. It is excellent
against rheumatoid arthritis, at least in animals. We worked together with
a London groupreal top of the field people in rheumatoid
arthritisand they have never seen anything as good as that. So chances
are that this particular compound, cannabidiol, can be used in rheumatoid
arthritis. And it has no psychotropic effects, as a matter of fact, because
it does not bind to the receptors. Maybe it has something to do with the
metabolism of anandamide. Maybe it blocks the anandamide breakdown. Maybe.
This is something we saw, but whether it's relevant to its activity, frankly
I don't know. So this compound possibly will be used for rheumatoid arthritis.
A company is already working on that ..." claims
Dr Raphael Mechoulam, as reported
by David Jay Brown,
"The
New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael
Mechoulam".

2004: "A drug made from an extract of cannabis has helped to reduce
the pain caused by rheumatoid arthritis. The drug, Sativex, has been developed
by GW Pharmaceuticals, which is assessing the medical benefits of cannabis
under a UK government licence. Tests of a spray form of the drug on 58 arthritis
patients showed it helped reduce pain, and improve quality of sleep. Few
people showed signs of side effects, the company said. ... Arthritis Research
Campaign ... spokeswoman said: 'It's not going to cure the disease, but it
will do a lot to allieviate the pain and suffering of people with rheumatoid
arthritis. Cannabis is probably less harmful than other available painkillers.
This idea that people with rheumatoid arthritis will be sitting around smoking
joints and getting high is quite wrong; cannabis-based pain killers should
be taken very seriously.' "  from
"Cannabis
drug cuts arthritis pain", BBC News, June 9 2004. Also see
news.bbc.co.uk/1/hi/health/3790227.stm,
Arthritis Research Campaign.

Autism

2009: "Cannabis has long-documented effects as an analgesic and an
anxiety modulator. Best of all, it is safe. ... with a few little [Marinol]
pills, everything turned around. But after about a week of playing around
with the dosage, J began garnering a few glowing school reports ...
The patients told me that Marinol couldnt compare to marijuana, the
plant, which has at least 60 cannabinoids to Marinols one. ... It's
strange, I've come to think, that the virtues of such a useful and harmless
botanical have been so clouded by stigma. Even the limited studies that have
been done suggest marijuana's potential as an adjunctive therapy for cancer.
... The drugs that our insurance would pay forand that the people around
us would support without questionpose real risks to children. For now,
were sticking with the weed."  "Why I Give My 9-year-old Pot" by
Marie Myung-Ok Lee, May 11 2009doublex.com/section/health-science/why-i-give-my-9-year-old-pot

2008: "Over a two-year period we did trials with Respirdol and Abilify
(atypical antipsychotics), Ritalin and Adderall (amphetamines), Prosac, Paxil
and Celexa (serotonin reuptake meds), and Tenex (Guanfacine), which is a
blood pressure medication. We have a cupboard full of prescriptions for Sam.
We tried different versions of the same type medications. We were encouraged
to keep trying a medication until we knew for sure it worked or didn't work.
The problem was he was having significant negative reactions to each medication
he would try. ... Sam had been having another horrible day before the dose.
After 30 minutes we could see the MC [Medical Cannabis] was beginning to
have an effect. Sams eyes got a little red and got a bit droopy. His
behavior became relaxed and far less anxious than he had been at the time
we gave him the MC. He started laughing for the first time in weeks. My wife
and I were astonished with the effect. It was as if all the anxiety, rage
and hostility that had been haunting him melted away. That afternoon and
evening his behavior was steady and calm. He started talking to us and
interacting with us again. Sams was physically more relaxed and began
initiating physical contact with the motivation being affection instead of
aggression. It was amazing! He went to sleep that night with no problem and
slept through the night. The MC continues to be a very effective medication.
Sam aggression has decrease dramatically.... Sam's life has improved dramatically
since he began using medical cannabis to treat his Autism Spectrum Disorder.
Because Sam is doing better, we are all doing better. We have our life's
back again."  "Using Medical Cannabis to Treat Autism Spectrum
Disorder"letfreedomgrow.com/cmu/SamsStory.htm

2003: "... a mother in Florida whose very large autistic son changed
from a sweet, loving boy to a teenager who flew into unpredictable rages
which 'were usually associated with self injury, aggression and property
damage.' She went on, 'At times I had to lock myself in the bathroom; otherwise
he would attack me. We gave him many medications, but nothing worked.' A
friend suggested a solution: a brownie with marijuana baked into it. 'Soon
after he ate the brownie,' she said, 'my son's anxiety disappeared, and his
sweet, loving behavior returned. He shows no signs of being under the influence
of a drug. He now receives one marijuana brownie and several doses of Marinol,
which contains the active ingredient in marijuana, each day. This has clearly
saved my child's life and my familys life.' ... Of all drugs, the
psychotropic drugs are among the least useful and most dangerous, and the
benefit/risk profile of medical marijuana seems fairly benign in comparison.
... 'I know it's not the end-all answer, but it's been the best answer for
the longest time for us in [comparison] to ALL the other medications. I cannot
tell you how many months we would go on a medication wondering if it
was doing anything at all. Here we can see the difference in 30 to 60 minutes.'
... 'My son (who is almost nine years old) has been on medications to
address his severe autistic behaviors ... None of the medications has
ever made a difference, except making his behaviors worse ... A few
months ago we tried the prescritipn drug Marinol and noticed a drop
in the severe epsiodes, no fits and little to no aggression toward his
teacher and family members on a daily basis. A few weeks ago we started
him on cannabis and stopped Marinol. Hew still has days when he gets
angry and moody, but we can adjust the dose to help him through those days
... I feel much more comfortable administering cannabis than something like
Riserdal.' "autism.com/ari/editorials/ed_marijuana.htm

2002: "She gave me some cupcakes and told me to give one to James
when life was tough, and if he needed it, give him another. Snap your fingers,
a miracle happened for us! No more rage, reduced anxiety, no constant deafening
noise and no house rocking and rolling. Those cupcakes had marijuana baked
into them. This marijuana was left over from a dying wolf dog named Sam.
Sam was the family pet, suffering with a brain tumor. My friend eased her
dying dog by putting marijuana into his food. The cupcakes were made with
left overs after Sam's dying. So, really, Sam saved my son's life, and our
family's life. My son now uses 2 1/2 mg of Marinol up to four times a day,
and one brownie up to four times a day. We try to keep the dose to a minimum,
because many days he is able to get by on less medication. When he has not
had enough medication we have Los Tormiento, a storm. We are able to recover
now, but in the past this was not the case. ... James D. has no discernible
side effects from the marijuana, and that cannot be said about previous
medications we have tried. Most of the drugs used for behavioral control
with the developmentally disabled are riddled with side effects, whether
an SSRI (luvox, celexa, paxil), or one of the anti-psychotic/tranquilizers
(Haldol, Risperdal, Thorazine); sometimes Ritalin and blood pressure medications
are added. ... her son's use of cannabis, recommended by a physician, comes
after years of trial and failure of conventional psychotropic medications,
diet, holistic medicine, behavior modification and other therapies. ... the
boy ate portions of muffins that had been prepared with marijuana. 'Within
half an hour, actually 35 minutes, of the first dose, it was a miracle,'
she said."  "The Sam Project: James D."letfreedomgrow.com/articles/james_d.htm

Botany

2005: "AS POLICE and dope smokers know, there are two types of cannabis.
Cannabis sativa sativa is mainly used to make hemp, while the indica subspecies
is prized for its tetrahydrocannabinol (THC) content, which produces the
'high'. But now Australian researchers have discovered a third type of cannabis,
called rasta. Simon Gilmore of the Canberra Institute of Technology catagorised
196 sample plants according to the DNA in their mitochondria and chloroplasts.
The samples included plants grown for drugs and hemp as well as wild varieties
from Europe, Asia, Africa, Mexico and Jamaica. The results showed three distinct
'races' of cannabis. In central Asia the THC-rich indica predominated, while
in western Europe sativa was more common. In India, south-east Asia, Africa,
Mexico and Jamaica the rasta variant predominated. It looks similar to the
sativa subspecies, but generally contains higher levels of THC." 
"Rasta
lends its name to a third type of cannabis", New Scientist, Sept
20 2005, pg 12.(Editor's note: "Rasta" is actually a fourth strain of cannabis. The third
strain is called "Ruderalis" and is native to Russia.)

Brain

2013: "A new study from Harvard University may help dismiss concerns about the link between marijuana use and schizophrenia.
While many still debate the potential for marijuana to cause schizophrenia, researchers at Harvard Medical School say there has
'yet to be conclusive evidence that cannabis use may cause psychosis.' Their latest study, published last week in the journal Schizophrenia Research,
adds support to the role of genetic factors in schizophrenia, and that marijuana use alone does not increase the risk of developing the disorder.
'In summary, we conclude that cannabis does not cause psychosis by itself. In genetically vulnerable individuals,
while cannabis may modify the illness onset, severity and outcome, there is no evidence from this study that it can cause the psychosis.'
The team, led by Lynn DeLisi, MD, Professor of Psychiatry at Harvard Medical School, compared the family histories of
108 schizophrenia patients and 171 individuals without schizophrenia to determine whether cannabis use was a factor in developing the disorder.
They found that a family history of schizophrenia increased the risk of developing schizophrenia,
regardless of whether or not an individual used cannabis. The authors say further studies should investigate whether marijuana can interact with
genetic factors to affect the age at which schizophrenia develops. However, the latest findings provide enough evidence for
Dr. DeLisi and her team to conclude that cannabis 'is unlikely to be the cause of illness.' ""Marijuana Does Not Cause Schizophrenia, Harvard Study Finds"
by Leaf Science, Dec 8 2013

2010: "A combination of compounds in marijuana could help fight off
a particularly deadly form of brain cancer,
preliminary research suggests. Researchers at the California Pacific Medical
Center Research Institute (CPMCRI) combined the non-psychoactive Cannabis
compound, cannabidiol (CBD), with
9-tetrahyrdocannabinol (9-THC), the primary psychoactive
active ingredient in Cannabis. They found the combination boosts the inhibitory
effects of 9-THC on glioblastoma, the most common and aggressive form of
brain tumor. 'Our study not only suggests that combining these two compounds
creates a synergistic effect but it also helps identify molecular mechanisms
at work here, and that may lead to more effective treatments for glioblastoma
and potentially other aggressive cancers', said Sean McAllister, a scientist
at CPMCRI and the lead author of the study." 
"Marijuana
compounds may help fight brain cancer", Jan 16 2010

2009: "Functional neuroimaging studies suggest a modulation of global
and prefrontal metabolism both during the resting state and after the
administration of THC/marijuana cigarettes. Minimal evidence of major effects
of cannabis on brain structure has been reported." 
"Neuroimaging
in cannabis use: a systematic review of the literature" by R Martin-Santos,
A B Fagundo, J A Crippa, Z Atakan, S Bhattacharyya, P Allen, P Fusar-Poli,
S Borgwardt, M Seal, G F Busatto, P McGuire, Psychological Medicine,
July 23 2009, pgs 1-17

2007: "Smoking pot won't make you crazy, but trying to find the truth
behind the recent rash of headlines regarding a supposed link between cannabis
and mental illness might. According to the Associated Press and other news
sources, a new study in the British medical journal The Lancet reports
that smoking cannabis  even occasionally  can increase one's
risk of becoming psychotic. It sounds alarming at first, but a closer look
at the evidence reveals that there's less here than the headlines imply.
First, there is no new study. The paper published in The Lancet is
a meta-analysis  a summary of seven studies that previously appeared
in other journals, including some that were published decades ago. Second,
the touted association between cannabis and mental illness is smallabout
the same size as the link between head injury and psychosis. Finally, despite
what some new sources suggest, this association is hardly proof of a
cause-and-effect relationship between cannabis and psychosis ... In fact,
investigators actually reported that cannabis use was associated with a slight
increase in psychotic outcomes. However, the authors emphasized (even if
many in the media did not) that this small association does not reflect a
causal relationship. Cannabis use can correlate with mental illness for many
reasons. People often turn to cannabis to alleviate the symptoms of distress.
A recent study performed in Germany showed that cannabis offsets certain
cognitive declines in schizophrenic patients. Another study shows that psychotic
symptoms predict later use of cannabis, suggesting that people might turn
to the plant for help rather than become ill after use. Perhaps the most
impressive evidence against the cause-and-effect relationship concerns the
unvarying rate of psychoses across different eras and different countries.
People are no more likely to be psychotic in Canada or the United States
(two nations where large percentages of citizens use cannabis) than they
are in Sweden or Japan (where self-reported marijuana use is extremely low).
Even after the enormous popularity of cannabis in the 1960s and 1970s, rates
of psychotic disorders haven't increased." 
"Interpreting
Hazy Warnings About Pot and Mental Illness" by
Paul Armentano, Mitch Earleywine,
Aug 7 2007.

2007: "There was an increased risk of any psychotic outcome in individuals
who had ever used cannabis. Findings were consistent with a dose-response
effect, with greater risk in people who used cannabis most frequently. Results
of analyses restricted to studies of more clinically relevant psychotic disorders
were similar. Depression, suicidal thoughts, and anxiety outcomes were examined
separately. Findings for these outcomes were less consistent, and fewer attempts
were made to address non-causal explanations, than for psychosis. A substantial
confounding eff ect was present for both psychotic and affective outcomes.
Interpretation: The evidence is consistent with the view that cannabis increases
risk of psychotic outcomes independently of confounding and transient
intoxication effects, although evidence for aff ective outcomes is less strong.
The uncertainty about whether cannabis causes psychosis is unlikely to be
resolved by further longitudinal studies such as those reviewed here. However,
we conclude that there is now suffi cient evidence to warn young people that
using cannabis could increase their risk of developing a psychotic illness
later in life." 
"Cannabis use
and risk of psychotic or affective mental health outcomes: a systematic
review", by Theresa H M Moore, Stanley Zammit, Anne Lingford-Hughes,
Thomas R E Barnes, Peter B Jones, Margaret Burke, Glyn Lewis, The
Lancet, 370: pgs 319-328, 2007.

2006: "U.S. scientists have discovered the active ingredient in marijuana
interferes with synchronized activity between neurons in the hippocampus
of rats. The authors suggest action of tetrahydrocannabinol, or THC, might
explain why marijuana impairs memory. Gyorgy Buzsaki and colleagues at Rutgers
University recorded the activity of multiple neurons in the hippocampus of
rats. Normally neurons in that region form groups that fire action potentials,
or nerve impulses, together at about 4-10 times per second. But when the
authors injected THC, or a related synthetic drug, into the hippocampus,
that synchrony was disrupted. The researchers said the drugs did not change
the total number of action potentials produced, just their tendency to occur
at the same time. Animals with less synchronized neural activity under the
drug performed less well in a standard test of memory, suggesting synchronized
neural firing is important for normal hippocampal function." 
"Study:
Marijuana may affect neuron firing", Nov 29 2006

2006: "Cannabinoids impair hippocampus-dependent memory in both humans
and animals, but the network mechanisms responsible for this effect are unknown.
Here we show that the cannabinoids 9-tetrahydrocannabinol and CP55940 decreased
the power of theta, gamma and ripple oscillations in the hippocampus of
head-restrained and freely moving rats. These effects were blocked by a CB1
antagonist. The decrease in theta power correlated with memory impairment
in a hippocampus-dependent task. By simultaneously recording from large
populations of single units, we found that CP55940 severely disrupted the
temporal coordination of cell assemblies in short time windows (<100 ms)
yet only marginally affected population firing rates of pyramidal cells and
interneurons. The decreased power of local field potential oscillations
correlated with reduced temporal synchrony but not with firing rate changes.
We hypothesize that reduced spike timing coordination and the associated
impairment of physiological oscillations are responsible for cannabinoid-induced
memory deficits." claims David Robbe, Sean M Montgomery, Alexander Thome,
Pavel E Rueda-Orozco, Bruce L McNaughton, György Buzsaki,
"Cannabinoids
reveal importance of spike timing coordination in hippocampal function",
Nov 19 2006

2006: "Although differences were observed between subjects who used
cannabis during adolescence and those who did not, no finding indicated
pathological change. Regions of higher ADC, putative evidence of atrophy,
were not present, although regions of significantly lower ADC were. While
low FA would be indicative of less white matter integrity, particularly with
respect to fiber direction, all FA differences in this study were higher
values in cannabis users than non-users. ... Thus, these data lead to the
likely conclusion that cannabis use, in at least moderate amounts, during
adolescence does not appear to be neurotoxic ..." claims Lynn E DeLisi, Hilary
C Bertisch, Kamila U Szulc, Magda Majcher, Kyle Brown, Arthika Bappal, Babak
A Ardekani, "A
preliminary DTI study showing no brain structural change associated with
adolescent cannabis use", Harm
Reduction Journal, May 9 2008

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin,
cocaine, and the more common
alcohol and nicotine 
inhibit the growth of these new cells. It was thought that marijuana did
the same thing, but this new research suggests otherwise. ... The researchers
found that rats treated with HU-210 [a potent synthetic cannabinoid] on a
regular basis showed neurogenesis  the growth of new brain cells in
the hippocampus. A current hypothesis suggests depression may be triggered
when the hippocampus grows insufficient numbers of new brain cells. If true,
HU-210 could offer a treatment for such mood disorders by stimulating this
growth." reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2005: "The relentless influx of emails, cellphone calls and instant
messages received by modern workers can reduce their IQ by more than smoking
marijuana, suggests UK research. ... says Glenn Wilson, a psychiatrist at
the University of London, UK, who carried out the study, sponsored by
Hewlett-Packard." reports Will Knight from
"'Info-mania'
dents IQ more than marijuana", New Scientist, Apr 22 2005

2004: "After studying more than 2000 users and non-users aged between
14 and 24, Jim van Los of the University of Maastricht in the Netherlands
concludes ... 21 per cent of cannabis users in his sample had psychotic symptoms,
compared with 15 per cent of non-users. The more often people used cannabis,
the stronger the effect. The risk appears greatest for those with a
predisposition to psychosis. In people with mild signs of psychosis at the
start of the study, 51 per cent of users developed symptoms compared with
26 per cent of non-users. However, several other reviews have come to a different
conclusion. In 1998, a French government study found that cannabis was the
least dangerous of all potentially addictive drugs." 
"Cannabis
use linked to psychotic experiences", New Scientist, Dec 4 2004,
pg 5.

2004: "A cannabis-like substance produced by the brain may dampen
delusional or psychotic experiences, rather than trigger them. Heavy cannabis
use has been linked to psychosis in the past, leading researchers to look
for a connection between the brain's natural cannabinoid system and
schizophrenia. Sure enough, when Markus Leweke of the University of Cologne,
Germany, and Andrea Giuffrida and Danielle Piomelli of the University of
California, Irvine, looked at levels of the natural cannabis-like substance
anandamide, they were higher in people with schizophrenia than in healthy
controls. The team measured levels of anandamide in the cerebrospinal fluid
(CSF) of 47 people suffering their first bout of schizophrenia, but who had
not yet taken any drugs for it, and 26 people who had symptoms of psychosis
and have a high risk of schizophrenia. Compared with 84 healthy volunteers,
levels were six times as high in people with symptoms of psychosis and eight
times as high in those with schizophrenia. 'This is a massive increase in
anandamide levels,' Leweke told the National Cannabis and Mental Illness
Conference in Melbourne, Australia, last week. And that is just in the CSF.
Levels could be a hundred times higher in the synapses, where nerve signalling
is taking place, he says. ... But were the high anandamide levels triggering
the psychotic symptoms or a response to them? Leweke and his colleagues found,
to their surprise, that the more severe people's schizophrenia was the lower
their anandamide levels. The team's theory is that rather than triggering
psychosis, the substance is released in response to psychotic symptoms to
help control them. People with the worst symptoms might be unable to produce
sufficient anandamide to prevent them. At some point in their lives, between
5 and 30 per cent of healthy people have had symptoms such as delusions or
hallucinations, which can be triggered by something as simple as sleep
deprivation. 'All of us are potentially psychotic,' says David Castle of
the University of Melbourne. So for the body to have a system that prevents
these experiences getting out of hand makes sense, he says. ... The new findings
suggest antipsychotic drugs could be developed that target the anandamide
system, but it will not be simple. The active ingredient in cannabis, THC,
binds to anandamide receptors. But people with schizophrenia who use cannabis
actually have more severe and frequent psychotic episodes than those who
do not. This may be because THC makes anandamide receptors less sensitive.
Leweke's team also found anandamide levels lowest in people with schizophrenia
who used cannabis more frequently, suggesting it may disrupt the system in
other ways too. Up to 60 per cent of people with schizophrenia use cannabis.
A study by Castle, also reported at the Melbourne meeting, has found that
people use the drug to get rid of unpleasant emotions associated with the
disease such as anxiety and depression." reports Rachel Nowak from
"Brain may produce
its own antipsychotic drug", New Scientist, Aug 30 2004.

2003: "Smoking marijuana will certainly affect perception, but it
does not cause permanent brain damage, researchers from the University of
California at San Diego said Friday in a study. 'The findings were kind of
a surprise. One might have expected to see more impairment of higher mental
function,' said Dr. Igor Grant, a UCSD professor of psychiatry and the study's
lead author. Other illegal drugs, or even alcohol,
can cause brain damage. His team analyzed data from 15 previously published,
controlled studies into the impact of long-term, recreational cannabis use
on the neurocognitive ability of adults. The studies tested the mental functions
of routine pot smokers, but not while they were actually high, Grant said.
The results, published in the July issue of the Journal of the International
Neuropsychological Society, show that marijuana has only a marginally
harmful long-term effect on learning and memory. No effect at all was seen
on other functions, including reaction time, attention, language, reasoning
ability, and perceptual and motor skills. ... The UCSD analysis of studies
involving 704 long-term cannabis users and 484 nonusers was sponsored by
a state-supported program that oversees research into the use of cannabis
to treat certain diseases. ... The UCSD research team said the problems observed
in learning and forgetting suggest that long-term marijuana use results in
selective memory defects, but said the impact was of a very small magnitude.
'If we barely find this tiny effect in long-term heavy users of cannabis,
then we are unlikely to see deleterious side effects in individuals who receive
cannabis for a short time in a medical setting,' Grant said." reports
Walter Cronkite,
"Pot Doesn't
Harm Brain, Study Shows", June 30 2003

2002: "The link between regular cannabis use and later depression
and schizophrenia has been significantly strengthened by three new studies.
... One of the key conclusions of the research is that people who start smoking
cannabis as adolescents are at the greatest risk of later developing mental
health problems. Another team calculates that eliminating cannabis use in
the UK population could reduce cases of schizophrenia by 13 per cent. Until
now, say Rey and Tennant, there was 'a dearth of reliable evidence' to support
the idea that cannabis use could cause schizophrenia or depression. That
lack of good evidence 'has handicapped the development of rational public
health policies,' according to one of the research groups, led by George
Patton at the Murdoch Children's Research Institute in Melbourne, Australia.
The reason for the link is unclear. Social consequences of frequent cannabis
use include educational failure and unemployment, which could increase the
risk of depression. "However, because the risk seems confined largely to
daily users, the question about a direct pharmacological effect remains,"
says Patton. ... The new analysis revealed a dose-dependant relationship
between the frequency of cannabis use and schizophrenia. This held true in
men with no psychotic symptoms before they started using cannabis, suggesting
they were not self-medicating. Finally, researchers led by Terrie Moffitt
at King's College London, UK, analysed comprehensive data on over 1000 people
born in Dunedin, New Zealand in 1972 and 1973. They found that people who
used cannabis by age 15 were four times as likely to have a diagnosis of
schizophreniform disorder (a milder version of schizophrenia) at age 26 than
non-users. But when the number of psychotic symptoms at age 11 was controlled
for, this increased risk dropped to become non-significant. This suggests
that people already at greater risk of later developing mental health problems
are also more likely to smoke cannabis. The total number of high quality
studies on cannabis use and mental health disorders remains small, stress
Rey and Tennant. And it is still not clear whether cannabis can cause these
conditions in people not predisposed by genetic factors, for example, to
develop them." claims Emma Young from
"Cannabis
link to mental illness strengthened", New Scientist news service,
Nov 21 2002.

2002: "Current marijuana use had a negative effect on global IQ score
only in subjects who smoked 5 or more joints per week. A negative effect
was not observed among subjects who had previously been heavy users but were
no longer using the substance. We conclude that marijuana does not have a
long-term negative impact on global intelligence. Whether the absence of
a residual marijuana effect would also be evident in more specific cognitive
domains such as memory and attention remains to be ascertained. ... For
comparison, an IQ decrement of 5 points has been observed in children exposed
prenatally to 3 alcoholic drinks per day, of 3.75 points in offspring exposed
prenatally to cocaine and of 2.6 points after low
lead exposure. ... Although the heavy current users experienced a decrease
in IQ score, their scores were still above average at the young adult assessment
(mean 105.1). If we had not assessed preteen IQ, these subjects would have
appeared to be functioning normally. Only with knowledge of the change in
IQ score does the negative impact of current heavy use become apparent."
claims Peter Fried, Barbara Watkinson, Deborah James, and Robert Gray, "Current
and former marijuana use: preliminary findings of a longitudinal study of
effects on IQ in young adults," Canadian Medical Association Journal,
Apr 2 2002, 166(7), pg 887, 890.

2002: "Do decades of dope-smoking wreck cannabis users' memory and
concentration? Or is this just another anti-marijuana myth? This long-running
debate reopened this week with the publication of a US government-funded
study which claims that smoking cannabis daily for 20 years or more impairs
memory and attention. Its findings are contradicted by others that have revealed
no long-term effects. The latest research involved 102 cannabis smokers in
Seattle, Farmington in Connecticut and Miami. Half had smoked for an average
of 24 years. The other half, described as 'short-term'users, had smoked for
10 years on average. Both groups reported smoking about two joints a day.
In tests such as memorising a list of 15 words, the long-term users recalled
8.5 words on average, 2.5 fewer than both the short-term users and 31 non-users.
The long-term users were also slower at mental arithmetic. But in in other
tasks, such as sorting cards, they were just as quick. claims Kurt Kleiner
from
"The
war on weed: Controversy still rages over whether cannabis damages the
brain", New Scientist news service, Mar 9 2002.

2002: "The neuroprotective effect of cannabinoids may have potential
clinical relevance for the treatment of neurodegenerative disorders such
as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson's
disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and
Patrick Weydt from
"Cannabis:
Old medicine with new promise for neurological disorders"

2001: "I am the mother of a 21-year-old male who was diagnosed with
a serious mental illness at 17 years. He had suffered with this illness since
5th grade, a thought disorder that he is unable to control which includes
suicidal thoughts. ... After three different facilities and uncountable
medications, different opinions, no has really said they had treated this
condition. [This condition] usually comes into view when the person is on
death row. ... He has been on medications that caused him to be unable to
read due to loss of vision, medications that made him more paranoid, to be
incontinent, to be unable to function. ... Out of desperation to be free
of the prison his mind creates at times, he smoked marijuana and says it
is the only time he is totally free of these thoughts. ... He seriously uses
this with a couple of other meds daily with good results. He doesn't stumble
around or look dazed. He is clear-eyed and plain spoken.... There has not
to my knowledge ever been a death recorded from this drug, but
alcohol and cigarettes have
killed many. ...If this one plant that God created for us can be used, let's
not withhold it causing undue stress and paranoid feelings for these people."
claims anonymous mother from
"Patient
Story - Mental Illness", June 26 2001.

1999: "There were no significant differences in cognitive decline
between heavy users, light users, and nonusers of cannabis. There were also
no male-female differences in cognitive decline in relation to cannabis use.
The authors conclude that over long time periods, in persons under age 65
years, cognitive decline occurs in all age groups. This decline is closely
associated with aging and educational level but does not appear to be associated
with cannabis use." claims Constantine G Lyketsos, Elizabeth Garrett, Kung-Yee
Liang, and James C Anthony,
"Cannabis
Use And Cognitive Decline In Persons Under 65 Years Of Age", American
Journal of Epidemiology, vol 149, no 9, pgs 794-800.

1998: "The neuroprotective actions of cannabidiol and other cannabinoids
were examined in rat cortical neuron cultures exposed to toxic levels of
the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced
by both cannabidiol, a nonpsychoactive constituent of marijuana, and the
psychotropic cannabinoid delta-9-tetrahydrocannabinol (THC). Cannabinoids
protected equally well against neurotoxicity mediated by N-methyl-D-aspartate
receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors,
or kainate receptors. N-methyl-D-aspartate receptor-induced toxicity has
been shown to be calcium dependent; this study demonstrates that
2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type
neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive
calcium channels. The neuroprotection observed with cannabidiol and THC was
unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid
receptor independent. Previous studies have shown that glutamate toxicity
may be prevented by antioxidants. Cannabidiol, THC and several synthetic
cannabinoids all were demonstrated to be antioxidants by cyclic voltametry.
Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative
damage as well as or better than other antioxidants in a chemical (Fenton
reaction) system and neuronal cultures. Cannabidiol was more protective against
glutamate neurotoxicity than either ascorbate or -tocopherol, indicating
it to be a potent antioxidant. These data also suggest that the naturally
occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially
useful therapeutic agent for the treatment of oxidative neurological disorders
such as cerebral ischemia." reports AJ Hampson, M Grimaldi, J Axelrod, D
Wink from
"Cannabidiol
and delta-9-tetrahydrocannabinol are neuroprotective antioxidants",
Proceedings of the National Academy of Sciences (PNAS), vol 95, no
14, July 7 1998.

1996: "Myth: Marijuana causes brain damage. The truth: This claim
is bases on a 20-year-old study in which two rhesus monkeys were exposed
to continuous massive doses of THC  up to 200 times the psychoactive
dose for humans. It has never been replicated, and there is no evidence anywhere
that marijuana users suffer brain damage." claims
Ira Glasser, Executive Director, American
Civil Liberties Union, from "More Reefer Madness" by Glasser, Visions
of Liberty #8, Aug. 25, 1996.

1991: Dr. David Blum of UCLA claims a Partnership for a Drug Free
America (PDFA) Public Service Announcement (PSA) that shows a near-flatline
brainwave electroencephalogram (EEG) of a cannabis user is not accurate.
Dr. Blum is one of several doctors to complain that the brainwaves in the
PDFA PSA were not those of a cannabis user. The producer of the PDFA PSA
admits the EEG is actually that of a person in a coma or unconscious, but
claims that, in a drug war, the "ends justify the means".

1991: Experimental exposure to cannabis smoke "does not compromise
the general health of the rhesus monkey." concludes a study headed by Dr.
William Slikker, Jr. at the National Center for Toxicological Research in
Arkansas. The study failed to find any evidence of brain damage in rhesus
monkeys exposed to cannabis. "Chronic Marijuana Smoke Exposure in the Rhesus
Monkey", by William Slikker, Jr,
et al, Fundamental and Applied Toxicology, #17, 1991, pgs. 321-322.

1989: "Whether the drug causes brain or other physical damage is much
debated." claims American Medical Association Home Medical Encyclopedia,
published by Reader's Digest, 1989.

1987: "... there are several reports of damaged brain cells and changes
in brainwave readings in monkeys smoking marijuana, but neurological and
neuropsychological tests in Greece, Jamiaca, and Costa Rica found no evidence
of functional brain damage." claims
Lester A Grinspoon, M.D.,
"Marijuana", The Harvard Medical School Mental Health Letter, Nov.
1987, pg. 3.

1978: "Federally funded studies of long-tern users of high-potency
marijuana in three foreign countries showed no difference between the health,
ability to work, and brain function of users and non-users, a number of
researchers said ... Dr Max Fink of department of psychiatry of the State
University of New York at Stoney Brook ... and ... Dr Alfred M Freedman,
insisted all the results clearly showed that there is no brain damage from
long-term marijuana smoking. ... Drs Paul Satz and Jack M Fletcher of the
University of Florida and Louis W Sutker of University of Victoria found
after giving 17 psychological and brain function tests to 41 users that '
chronic marijuana use is not associated with permanent or irreversible impairment
in high brain functions or intelligence.' " reports Stuart Auerbach in "Studies
See No Health Effect of Pot Smoking, Researchers Say", Washington Post, Jan
28 1978.

"For THC, the cannabinoid synthesized by cannabis sativa and indica, and
andandamide, the cannabinoid synthesized in the central nervous systems of
most animals on Earth, the receptor antagonist is called SR141716. SR141716
is like 'anti-marijuana'  it enhances the same memory functions that
the natural brain cannabinoid anandamide and THC inhibit through the cannabinoid
receptor. SR141716 improves short term memory in rodents by blocking the
CB1 cannabinoid receptor from binding to andandamide, not just THC. But
anandamide is made by the brain naturally. Why would the brain be making
a chemical  andandamide  that seems to inhibit short-term memory?
This question is partly answered by the effect of SR141716 on the sleep cycles
of rats. SR141716 administered to rats interrupts their sleep cycles, causing
a deficit in both short-wave and REM sleep. This research indicates that
cannabinoids are important in the brain's regulation of the sleeping process.
The cost of improving short-term memory by blocking cannabinoids from the
brain is deficient and delayed slow-wave and REM sleep. In studying marijuana,
we have learned something important about the brain. Inhibition of short-term
memory-related processes occurring ion the hippocampus might be necessary
for a healthy sleep cycle." claims Los Angeles Cannabis Resource Center
from "Cannabinoids
in the brain".

Cancer

2010: "A combination of compounds in marijuana could help fight off
a particularly deadly form of brain cancer, preliminary research suggests.
Researchers at the California Pacific Medical Center Research Institute (CPMCRI)
combined the non-psychoactive Cannabis compound, cannabidiol (CBD), with
9-tetrahyrdocannabinol (9-THC), the primary psychoactive active ingredient
in Cannabis. They found the combination boosts the inhibitory effects of
9-THC on glioblastoma, the most common and aggressive form of brain tumor.
'Our study not only suggests that combining these two compounds creates a
synergistic effect but it also helps identify molecular mechanisms at work
here, and that may lead to more effective treatments for glioblastoma and
potentially other aggressive cancers', said Sean McAllister, a scientist
at CPMCRI and the lead author of the study." 
"Marijuana
compounds may help fight brain cancer", Jan 16 2010

2007: "Cannabis may be bad for the lungs, but the active ingredient
in marijuana may help combat lung cancer, new research suggests. In lab and
mouse studies, the compound, known as THC, cut lung tumor growth in half
and helped prevent the cancer from spreading, says Anju Preet, PhD, a Harvard
University researcher in Boston who tested the chemical. ... Moreover, other
early research suggests the cannabis compound could help fight brain, prostate,
and skin cancers as well, Preet says. The findings were presented at the
annual meeting of the American Association for Cancer Research. THC seeks
out, attaches to, and activates two specific endocannabinoids that are present
in high amounts on lung cancer cells, Preet says. This revs up their natural
anti-inflammatory properties. Inflammation can promote the growth and spread
of cancer. In the new study, the researchers first demonstrated that THC
inhibited the growth and spread of cells from two different lung cancer cell
lines and from patient lung tumors. Then, they injected THC into mice that
had been implanted with human lung cancer cells. After three weeks, tumors
shrank by about 50%, compared with tumors in untreated mice." reports Charlene Laino from
"Marijuana May Fight Lung Tumors", Apr 17 2007
also see norml.org/news/2007/04/19/pot-s-active-ingredient-halts-lung-cancer-growth-study-says, Apr 19 2007

2006: "delta-9-tetrahydrocannabinol (THC) exhibits anti-tumor effects
on various cancer cell types, but its use in chemotherapy is limited by its
psychotropic activity. We investigated the anti-tumor activities of other
plant cannabinoids, i.e. cannabidiol, cannabigerol, cannabichromene,
cannabidiol-acid and THC-acid, and assessed whether there is any advantage
in using Cannabis extracts (enriched in either cannabidiol or THC) over pure
cannabinoids. Results obtained in a panel of tumor cell lines clearly indicate
that, of the five natural compounds tested, cannabidiol is the most potent
inhibitor of cancer cell growth (IC50 between 6.0 and 10.6 µM),
with significantly lower potency in noncancer cells. The cannabidiol-rich
extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene
followed in the rank of potency. Both cannabidiol and the cannabidiol-rich
extract inhibited the growth of xenograft tumors obtained by subcutaneous
injection into athymic mice of human MDA-MB-231 breast carcinoma or rat
v-K-ras-transformed thyroid epithelial cells, and reduced lung metastases
deriving from intra-paw injection of MDA-MB-231 cells. Judging from several
experiments on its possible cellular and molecular mechanisms of action,
we propose that cannabidiol lacks a unique mode of action in the cell lines
investigated. At least for MDA-MB-231 cells, however, our experiments indicate
that cannabidiol effect is due to its capability of inducing apoptosis via:
1) direct or indirect activation of cannabinoid CB2 [cannabinoid
receptor type-2] and vanilloid TRPV1 [transient receptor potential vanilloid
type-1] receptors; and 2) cannabinoid/vanilloid receptor-independent elevation
of intracellular Ca2+ and reactive oxygen species. Our data support
the further testing of cannabidiol and cannabidiol-rich extracts for the
potential treatment of cancer. ... In conclusion, our data indicate that
cannabidiol, and possibly Cannabis extracts enriched in this natural cannabinoid,
represent a promising non-psychoactive antineoplastic strategy. In particular,
for a highly malignant human breast carcinoma cell line we have shown here
that cannabidiol and a cannabidiol-rich extract counteract cell growth both
in vivo and in vitro as well as tumor metastasis in vivo. Cannabidiol exerts
its effects on these cells through a combination of mechanisms that include
either direct or indirect activation of CB2 and TRPV1 receptors,
and induction of oxidative stress, all contributing to induce apoptosis.
Additional investigations are required to understand the mechanism of the
growth inhibitory action of cannabidiol in the other cancer cell lines studied
here." claim Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz,
Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe
Portella, Maurizio Bifulco, Vincenzo Di Marzo,
"Anti-tumor
activity of plant cannabinoids with emphasis on the effect of cannabidiol
on human breast carcinoma", Endocannabinoid Research Group, Istituto
di Chimica Biomolecolare, CNR Pozzuoli, Italy, May 25 2006.

2005: "Controlled studies have revealed therapeutic utility of
cannabinoids ... tumor retardation have also been shown. ... There are several
groups that have found it effective in reducing tumor growth. This is probably
due to the same mechanism as before with the neuroprotection. It's probably
not only neuroprotective; it's probably a protective agent in general. So,
to a certain extent, the endocannabinoid system can be compared with the
immune system. Now, the immune system obviously guards us against protein
effects, viruses, and microbes, but not all damages. So just as our body
protects itself with the immune system against microbes or viruses, it also
tries to protect itself with other systemsand the endocannabinoid system
is one of them. So I believe that it certainly acts against cancer cells.
There is a very important group in Spain that has done some excellent work
on that, and they're actually going into human work now with some cancers
found in the brain. We have also done a little bit on that, and there is
an Italian group that has done a lot of work on that. So, basically, it seems
that this is one of the routes that our body uses to try and protect itself
withby acting on cancers using several different mechanisms, not just
one." claims Dr Raphael Mechoulam,
as reported by David Jay Brown,
"The
New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael
Mechoulam".

2005: "Tashkin controlled
for tobacco use and calculated the relative risk of
marijuana use resulting in lung and upper airwaves cancers. All the odds
ratios turned out to be less than one (one being equal to the control group's
chances)! Compared with subjects who had used less than one joint year, the
estimated odds ratios for lung cancer were .78; for 1-10 j-yrs, .74; for
10-30 j-yrs, .85 for 30-60 j-yrs; and 0.81 for more than 60 j-yrs. The estimated
odds ratios for oral/pharyngeal cancers were 0.92 for 1-10 j-yrs; 0.89 for
10-30 j-yrs; 0.81 for 30-60 j-yrs; and 1.0 for more than 60 j-yrs. 'Similar,
though less precise results were obtained for the other cancer sites,' Tashkin
reported. ... There was time for only one question, said the moderator, and
San Francisco oncologist Donald
Abrams, M.D., was already at the microphone: 'You don't see any positive
correlation, but in at least one category [marijuana-only smokers and lung
cancer], it almost looked like there was a negative correlation, i.e., a
protective effect. Could you comment on that?' 'Yes,' said Tashkin. 'The
odds ratios are less than one almost consistently, and in one category that
relationship was significant, but I think that it would be difficult to extract
from these data the conclusion that marijuana is protective against lung
cancer. But that is not an unreasonable hypothesis.' " reports
Fred Gardner from
"Study:
Smoking Marijuana Does Not Cause Lung Cancer", CounterPunch, July
2-4 2005.

2004: "Clinical research touted by the journal of the American Association
for Cancer Research that shows marijuana's components can inhibit the growth
of cancerous brain tumors is the latest in a long line of studies demonstrating
the drug's potential as an anti-cancer agent. ... researchers at Madrid's
Complutense University that found cannabis restricts the blood supply to
glioblastoma multiforme tumors, an aggressive brain tumor ... the first
experiment documenting pot's anti-tumor effects took place in 1974 at the
Medical College of Virginia at the behest of the US government. The results
of that study, reported in an Aug. 18, 1974, Washington Post newspaper feature,
were that marijuana's psychoactive component, THC, 'slowed the growth of
lung cancers, breast cancers and a virus-induced leukemia in laboratory mice,
and prolonged their lives by as much as 36 percent.' ... secret - clinical
trial in the mid-1990s. That study, conducted by the US National Toxicology
Program to the tune of $2 million concluded that mice and rats administered
high doses of THC over long periods had greater protection against malignant
tumors than untreated controls. However, rather than publicize their findings,
government researchers shelved the results, which only became public after
a draft copy of its findings were leaked in 1997 to a medical journal which
in turn forwarded the story to the national media. ... In 1998, a research
team at Complutense's Department of Biochemistry and Molecular Biology discovered
that THC can selectively induce program cell death in brain tumor cells without
negatively impacting the surrounding healthy cells. Then in 2000, they reported
in the journal Nature Medicine that injections of synthetic THC eradicated
malignant gliomas (brain tumors) in one-third of treated rats, and prolonged
life in another third by six weeks. Last year, researchers at the University
of Milan in Naples, Italy, reported in the Journal of Pharmacology and
Experimental Therapeutics that non-psychoactive compounds in marijuana inhibited
the growth of glioma cells in a dose dependent manner, and selectively targeted
and killed malignant cells through a process known as apoptosis. And finally,
this month, researchers reported that marijuana's constituents inhibited
the spread of brain cancer in human tumor biopsies from patients who had
failed standard cancer therapies." reports
Paul Armentano from
"Report
Supressed That Marijuana Components Can Inhibit Cancer Growth",
Coastal Post, Oct 26 2004.

2004: "Who could imagine that cannabis might one day offer hope as
a cure for cancer? The United States government, thats who. ... recent
publication of a trio of clinical studies and a pair of scientific reviews
have effectively blown the lid off 'Cancergate,' and revealed that pots
medical value may be far greater than ever presumed. ... Last year, five
scientific journals published prominent articles trumpeting cannabinoids
(compounds in marijuana) as potential anti-cancer agents. ... the first ever
experiment documenting pots anti-tumor effects took place in 1974 at
the Medical College of Virginia at the behest of the U.S. government. The
results of that study, immortalized in an August 18, 1974 Washington
Post newspaper feature, were that 'THC slowed the growth of lung cancers,
breast cancers and a virus-induced leukemia in laboratory mice, and prolonged
their lives by as much as 36 percent.' ... Madrid, Spains Complutense
University, School of Biology ... led by investigator Manuel Guzman ... Guzman
believes that enough favorable clinical evidence exists supporting pots
anti-cancer properties to warrant clinical trials in humans. ... Guzman wrote
in the October 2003 issue of Nature Reviews Cancer. 'Anti-tumor compounds
should selectively affect tumor cells [and] it seems that cannabinoids can
do this, as they kill [malignant] tumor cells but do not affect their
non-transformed counterparts and might even protect them from cell death.
... As cannabinoids are relatively safe compounds, it would be desirable
that clinical trials using cannabinoids ... could accompany [ongoing] laboratory
studies to allow us to use these compounds in the treatment of cancer.' ...
'Cannabinoid research continues to show tremendous potential in the treatment
of cancer,' summarizes University of Southern California professor
Mitch Earleywine, author of the
book
Understanding
Marijuana: A New Look at the Scientific Evidence. ... 'Lets
hope that our drug policy wont stymie the battle against the second
leading cause of death in America.' Indeed. Lets not add a potential
treatment for cancer to the ever-growing list of victims of pot prohibition."
reports Paul Armentano from
"Unlocking a
Cure for Cancer  With Pot", Aug 17 2004.

2004: "Cannabinoids inhibit tumor angiogenesis in mice, but the mechanism
of their antiangiogenic action is still unknown. Because the vascular endothelial
growth factor (VEGF) pathway plays a critical role in tumor angiogenesis,
here we studied whether cannabinoids affect it. As a first approach, cDNA
array analysis showed that cannabinoid administration to mice bearing s.c.
gliomas lowered the expression of various VEGF pathway-related genes. The
use of other methods (ELISA, Western blotting, and confocal microscopy) provided
additional evidence that cannabinoids depressed the VEGF pathway by decreasing
the production of VEGF and the activation of VEGF receptor (VEGFR)-2, the
most prominent VEGF receptor, in cultured glioma cells and in mouse gliomas.
Cannabinoid-induced inhibition of VEGF production and VEGFR-2 activation
was abrogated both in vitro and in vivo by pharmacological blockade of ceramide
biosynthesis. These changes in the VEGF pathway were paralleled by changes
in tumor size. Moreover, intratumoral administration of the cannabinoid
9-tetrahydrocannabinol to two patients with glioblastoma multiforme (grade
IV astrocytoma) decreased VEGF levels and VEGFR-2 activation in the tumors.
Because blockade of the VEGF pathway constitutes one of the most promising
antitumoral approaches currently available, the present findings provide
a novel pharmacological target for cannabinoid-based therapies." claims Cristina
Blázquez, Luis González-Feria, Luis Álvarez, Amador
Haro, M Llanos Casanova, Manuel Guzmán from
"Cannabinoids
Inhibit the Vascular Endothelial Growth Factor Pathway in Gliomas",
Cancer Research #64, Aug 15 2004, pgs 5617-5623.

2002: "A study published in the July 2002 edition of the medical journal
Blood found that THC and some other cannabinoids produced 'programmed
cell death' in different varieties of human leukemia and lymphoma cell lines,
thereby destroying the cancerous cells but leaving other cells unharmed.
This reaffirms results by researchers at Madrid's Complutense University,
who destroyed otherwise uncurable brain cancer tumors in rats by injecting
them with THC." reports Dana Larsen,
"THC
destroys cancer cells, but the research is buried and ignored.", Sept
3 2002.

2002: "Before she [Franklyn
C Nofziger's daughter] died she underwent heavy chemotherapy [for her
lymphoma] that caused nausea, diarrhea and loss of appetite. None of the
legal medications including the marijuana substitute Marinol helped to alleviate
the symptoms. In desperation, we turned to marijuana to see if that would
help. Fortunately, people know a lot more about where to find marijuana than
people of my generation. And the marijuana did help reduce the side effects
of the chemotherapy to the point where she regained her appetite and actually
began putting on weight. Obviously, it did not save her life nor did we think
it would. However, it made a portion of the last weeks of her life considerably
more bearable both to her and to her family. Since then I have learned that
marijuana can also help persons with glaucoma, the wasting symptoms of AIDS,
multiple sclerosis and other afflictions. Because of this I have become an
avid supporter of efforts to legalize marijuana for medicinal purposes. An
administration that claims to be both compassionate and conservative should
enthusiastically support legislation that truly is compassionate and that
also returns rights to the states that the Tenth Amendment theoretically
guarantees to them."  claimed Franklyn C Nofziger,
"Former
Reagan Aide Among Medical Marijuana Supporters" by Jim Burns, July 25
2002

2001: "... researchers in Madrid announced they had destroyed incurable
brain cancer tumors in rats by injecting them with THC, the active ingredient
in cannabis. ... The Madrid researchers reported in the March [2000] issue
of "Nature
Medicine" that they injected the brains of 45 rats with cancer cells,
producing tumors whose presence they confirmed through magnetic resonance
imaging (MRI). On the 12th day they injected 15 of the rats with THC and
15 with Win-55,212-2 a synthetic compound similar to THC. All the rats left
untreated uniformly died 12-18 days after glioma (brain cancer) cell inoculation
... Cannabinoid (THC)-treated rats survived significantly longer than control
rats. THC administration was ineffective in three rats, which died by days
16-18. Nine of the THC-treated rats surpassed the time of death of untreated
rats, and survived up to 19-35 days. Moreover, the tumor was completely
eradicated in three of the treated rats." The rats treated with Win-55,212-2
showed similar results. The Spanish researchers, led by Dr. Manuel Guzman
of Complutense University, also irrigated healthy rats' brains with large
doses of THC for seven days, to test for harmful biochemical or neurological
effects. They found none." reports Raymond Cushing,
"Pot
Shrinks Tumors: Government Knew in 74"

2000: "Marijuana-like drugs eradicated some brain cancers in rats
and helped other animals live longer, possibly hinting at a new approach
for treating the disease ... The study dealt with gliomas, the most common
category of cancer arising in the brain. Gliomas are highly lethal in people
despite treatment with drugs, surgery and radiation. The rat study was published
in the March issue of the journal
Nature
Medicine. It was conducted by scientists at the Complutense and Autonoma
Universityersities in Madrid, Spain. They injected glioma cells into the
brains of rats to produce tumors. Untreated rats died within 18 days. Other
rats were treated with drug infusions for seven days through a tube leading
to the tumor. Fifteen rats got infusions of THC, the main active component
in marijuana. Tumors disappeared in three animals, and nine other rats outlived
the untreated ones, surviving up to 35 days. When researchers used a different
but similar drug, five of 15 rats became tumor-free and four others outlived
untreated animals."  Associated Press, "Dope Ingredient May Fight Cancer",
Feb 28, 2000.

1983: "[Inhaled] Marijuana has been shown to be effective for many
cancer chemotherapy patients, safe dosage levels have been established and
a dosage regimen which minimizes undesirable side effects has been devised
and tested." claims California Research Advisory Panel, Annual Report
of the California Research Advisory Panel, vol 14, submitted to the Governor
and Legislature.

1974: "In 1974 researchers at the Medical College of Virginia, who
had been funded by the National Institute of Health to find evidence that
marijuana damages the immune system, found instead that THC slowed the growth
of three kinds of cancer in mice  lung and breast cancer, and a
virus-induced leukemia. ... The DEA quickly shut down the Virginia study
and all further cannabis/tumor research, according to
Jack Herer ..." reports Raymond Cushing,
"Pot
Shrinks Tumors: Government Knew in 74",
americanmarijuana.org/pot.shrinks.tumors.html

2009: "Frequent and/or long-term marijuana use may significantly increase
a man's risk of developing the most aggressive type of testicular cancer,
according to a study by researchers at Fred Hutchinson Cancer Research Center.
The study results were published online Feb 9 in the journal Cancer.
The researchers found that being a marijuana smoker at the time of diagnosis
was associated with a 70 percent increased risk of testicular cancer. The
risk was particularly elevated (about twice that of those who never smoked
marijuana) for those who used marijuana at least weekly and/or who had long-term
exposure to the substance beginning in adolescence. The results also suggested
that the association with marijuana use might be limited to nonseminoma,
a fast-growing testicular malignancy that tends to strike early, between
ages 20 and 35, and accounts for about 40 percent of all testicular-cancer
cases. ... The researchers emphasize that their results are not definitive,
but rather open a door to more research questions. 'Our study is the first
inkling that marijuana use may be associated with testicular cancer, and
we still have a lot of unanswered questions,' [Stephen M] Schwartz said,
such as why marijuana appears to be associated with only one type of testicular
cancer. 'We need to conduct additional research to see whether the association
can be observed in other populations' ... The National Cancer Institute,
the National Institute on Drug Abuse and funds from the Hutchinson Center
supported this research ... According to the National Cancer Institute,
testicular cancer is very rare, accounting for only 1 percent of cancers
in U.S. men. About 8,000 men are diagnosed with testicular cancer each year,
and about 390 die of the disease annually." 
"Marijuana
Use Linked to Increased Risk of Testicular Cancer", Feb 9 2009. Related
articles:
"Association
of Marijuana Use and the Incidence of Testicular Germ Cell Tumors",
"Marijuana
Linked to Aggressive Testicular Cancer"

2008: "Smoking marijuana (cannabis) does not increase the user's risk
of head and neck cancer, according to a new study published in the March
2008 issue of Otolaryngology - Head and Neck Surgery. The small sample
study, authored by researchers from New Zealand and Great Britain, found
that among 75 cases of head and neck cancer, the relative risk of smoking
cannabis and contracting head and neck cancer in marijuana users was the
same (1.0) as in those who had never smoked cannabis. These results differ
from the relative risk of contracting cancer from smoking
[tobacco] cigarettes (2.1) and the heavy consumption
of alcohol (5.7), compared with those who abstained
from those activities." 
"Small
study shows marijuana does not increase risk of head, neck cancer", Mar
5 2008

2005: "Marijuana smoking -'even heavy longterm use'- does not cause
cancer of the lung, upper airwaves, or esophagus,
Donald Tashkin reported at this
year's meeting of the International Cannabinoid Research Society. Coming
from Tashkin, this conclusion had extra significance for the assembled
drug-company and university-based scientists (most of whom get funding from
the U.S. National Institute on Drug Abuse). Over the years, Tashkin's lab
at UCLA has produced irrefutable evidence of the damage that marijuana smoke
wreaks on bronchial tissue. With NIDA's support, Tashkin and colleagues have
identified the potent carcinogens in marijuana smoke, biopsied and made
photomicrographs of pre-malignant cells, and studied the molecular changes
occurring within them. It is Tashkin's research that the Drug Czar's office
cites in ads linking marijuana to lung cancer. Tashkin himself has long believed
in a causal relationship, despite a study in which Stephen Sidney examined
the files of 64,000 Kaiser patients and found that marijuana users didn't
develop lung cancer at a higher rate or die earlier than non-users. Of five
smaller studies on the question, only two -involving a total of about 300
patients concluded that marijuana smoking causes lung cancer. Tashkin
decided to settle the question by conducting a large, prospectively designed,
population-based, case-controlled study. 'Our major hypothesis,' he told
the ICRS, 'was that heavy, longterm use of marijuana will increase the risk
of lung and upper-airwaves cancers.' ... Exposure to marijuana was measured
in joint years (joints per day x 365). Controls were found based on age,
gender and neighborhood. Among them, 46% had never used marijuana, 31% had
used less than one joint year, 12% had used 10-30 j-yrs, 2% had used 30-60
j-yrs, and 3% had used for more than 60 j-yrs. Tashkin controlled for
tobacco use and calculated the relative risk of marijuana
use resulting in lung and upper airwaves cancers. All the odds ratios turned
out to be less than one (one being equal to the control group's chances)!
Compared with subjects who had used less than one joint year, the estimated
odds ratios for lung cancer were .78; for 1-10 j-yrs, .74; for 10-30 j-yrs,
.85 for 30-60 j-yrs; and 0.81 for more than 60 j-yrs. The estimated odds
ratios for oral/pharyngeal cancers were 0.92 for 1-10 j-yrs; 0.89 for 10-30
j-yrs; 0.81 for 30-60 j-yrs; and 1.0 for more than 60 j-yrs. ... 'So, in
summary' Tashkin concluded, 'we failed to observe a positive association
of marijuana use and other potential confounders.' " reports
Fred Gardner from
"Study:
Smoking Marijuana Does Not Cause Lung Cancer", CounterPunch, July
2-4 2005.

2004: "Previous laboratory investigations,
case reports, and a hospital-based case-control study have suggested that
marijuana use may be a risk factor for squamous cell head and neck cancer.
We conducted a population-based case-control study to determine whether marijuana
use is associated with the development of oral squamous cell carcinoma (OSCC).
Case subjects (n = 407) were 1865-year-old residents of three counties
in western Washington State who were newly diagnosed with OSCC from 1985
through 1995. Control subjects (n = 615), who were similar to the cases with
respect to age and sex, were selected from the general population using
random-digit telephone dialing. Lifetime histories of marijuana use and exposure
to known OSCC risk factors were ascertained using a structured questionnaire.
Information on genetic polymorphisms in glutathione S-transferase enzymes
was obtained from assays on participant DNA. Odds ratios for associations
with features of marijuana use were adjusted for sex, education, birth year,
alcohol consumption, and
cigarette smoking. A similar proportion of case subjects
(25.6%) and control subjects (24.4%) reported ever use of marijuana (adjusted
odds ratio, 0.9; 95% confidence interval, 0.61.3). There were no trends
in risk observed with increasing duration or average frequency of use or
time since first or last use. No subgroup defined by known or suspected OSCC
risk factors (age, cigarette smoking, alcohol consumption, and genetic
polymorphisms) showed an increased risk. Marijuana use was not associated
with OSCC risk in this large, population-based study." claims Karin A.
Rosenblatt1, Janet R. Daling2,3, Chu Chen2,3, Karen J. Sherman4 and Stephen
M. Schwartz, from
"Marijuana
Use and Risk of Oral Squamous Cell Carcinoma", Cancer Research #64,
June 1 2004, pgs 4049-4054.

2004: "Cannabinoids, the active components of
marijuana and their endogenous counterparts were reported as useful analgetic
agents to accompany primary cancer treatment by preventing nausea, vomiting,
and pain and by stimulating appetite. Moreover, they have been shown to inhibit
cell growth and to induce apoptosis in tumor cells. Here, we demonstrate
that anandamide, 9-tetrahydrocannabinol (THC), HU-210, and Win55,212-2 promote
mitogenic kinase signaling in cancer cells. Treatment of the glioblastoma
cell line U373-MG and the lung carcinoma cell line NCI-H292 with nanomolar
concentrations of THC led to accelerated cell proliferation that was completely
dependent on metalloprotease and epidermal growth factor receptor (EGFR)
activity. EGFR signal transactivation was identified as the mechanistic link
between cannabinoid receptors and the activation of the mitogen-activated
protein kinases extracellular signal-regulated kinase 1/2 as well as prosurvival
protein kinase B (Akt/PKB) signaling. Depending on the cellular context,
signal cross-communication was mediated by shedding of proAmphiregulin (proAR)
and/or proHeparin-binding epidermal growth factor-like growth factor (proHB-EGF)
by tumor necrosis factor converting enzyme (TACE/ADAM17). Taken together,
our data show that concentrations of THC comparable with those detected in
the serum of patients after THC administration accelerate proliferation of
cancer cells instead of apoptosis and thereby contribute to cancer progression
in patients." claims Stefan Hart, Oliver M Fischer, Axel Ullrich from
"Cannabinoids
Induce Cancer Cell Proliferation via Tumor Necrosis Factor -Converting Enzyme
(TACE/ADAM17)-Mediated Transactivation of the Epidermal Growth Factor
Receptor", Cancer Research #64, Mar 15 2004, pgs 1943-1950.
See another summary of the above article

2003: "Although the inhalation of chemical toxins in cannabis smoke
has been linked to bronchitis and other respiratory problems, it has not
been shown to cause lung cancer or a higher death rate. from
"Marijuana
Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Jouurnal
of the California Cannabis Research Medical Group, Summer 2003.

2000: "Marijuana, unlike tobacco and alcohol, does not appear to cause head,
neck, or lung cancer, says a researcher from Johns Hopkins Medical School
in Baltimore who presented findings from a study here recently at a meeting
of internal medicine physicians ... Daniel E. Ford, MD, tried to sort out
the evidence by the lifestyles  including marijuana, tobacco, and alcohol
use -- of 164 persons who were newly diagnosed with head, neck, or lung cancer
compared to a group of 526 healthy persons living in the same area. ... According
to Ford, he thought he would find an association between marijuana use and
cancer, but "that the association would fall away when we corrected for tobacco
use. That was not the case. The association was never there. 'And that surprised
him because of the way marijuana is smoked: deep inhalations, with the smoke
held in for effect. "It seemed natural that there would be some connection,'
he tells WebMD." reports Peggy Peck,
"Marijuana
Unlikely to Cause Head, Neck, or Lung Cancer", WebMD, May 8 2000

2000: "Stephen Sidney, MD, at the Division of Research, Kaiser Permanente
Medical Care Program, 3505 Broadway, Oakland, CA 94611 ... confirmed that
they found lower levels of cancer among the marijuana smokers when compared
to their control group." American Journal of Public Health.

1999: "Recent reports of molecular and genetic alterations in marijuana
users suggested that marijuana smoke might also activate CYP1A1 gene. Dr.
Roth investigated this possibility using Hepa-1 cells and found that marijuana
tar, and more specifically D9-THC, regulates the induction and function of
CYP1A1 gene, an observation that is entirely novel. Transcriptional activation
of CYP1A1 by D9-THC may help to explain the relatively high frequency of
DNA mutations and mucosal abnormalities that occur in marijuana smokers.
The inhalation of marijuana smoke delivers both nanogram concentrations of
conventional PAHs and milligram quantities of D9-THC to the lung. Induction
of CYP1A1 produced by D9-THC could result in greater activation of smoke-related
procarcinogens and higher adduct-related injury. However, it is also possible
that inhaled D9-THC competes for the active site of CYP1A1, paradoxically
reducing the activation of procarcinogens." claims Dr Michael D Roth from
"A Conference Summary
on Pulmonary Pathophysiologic and Immune Consequences of Smoked Substance
Abuse", National Institute on Drug Abuse.

1998: "I said, 'Do you know of any cases of marijuana-only smokers
who had lung cancer?' [Dr Donald
P Tashkin] said 'Yes, there is one.' Then he smiled, explaining,
'He was sixteen years old.' We both smiled, knowing a teenager could not
possibly have sufficient exposure to marijuana smoke to cause lung
cancerhis cancer was clearly due to some other cause." claims Martin
Martinez from
"Cannabis
and Lung Cancer".

1997: "Marijuana Use and Mortality", American Journal of Public
Health, April 1997.

1996: "THC was not mutagenic in Salmonella typhimurium strains TA97,
TA98, TA100, or TA1535 with or without rat and hamster liver S9 fractions.
In cultured Chinese hamster ovary cells, THC induced sister chromatid exchanges
at the highest dose tested in the presence of S9; at this dose level, cell
cycle delay indicative of toxicity was observed. THC did not induce chromosomal
aberrations in cultured Chinese hamster ovary cells with or without S9 metabolic
activation enzymes. In vivo, no increase in the frequency of micronucleated
erythrocytes was observed in the peripheral blood of male or female mice
administered THC by gavage for 13 weeks. ... Under the conditions of these
2-year gavage studies, there was no evidence of carcinogenic activity of
1-trans-delta9-tetrahydrocannabinol in male or female F344/N rats administered
12.5, 25, or 50 mg/kg. There was equivocal evidence of carcinogenic activity
of THC in male and female B6C3F1 mice based on the increased incidences of
thyroid gland follicular cell adenomas in 125 mg/kg groups. Increased incidences
of thyroid gland follicular cell hyperplasia occurred in male and female
mice, and increased incidences of hyperplasia and ulcers of the forestomach
were observed in male mice. The incidences of mammary gland fibroadenomas
and uterine stromal polyps were decreased in dosed groups of female rats,
as were the incidences of pancreatic adenomas, pituitary gland adenomas,
and interstitial cell adenomas of the testis in dosed male rats and liver
neoplasms in dosed mice. These decreases were likely related to lower body
weights in dosed animals." 
Abstract
of "TR-446:
Toxicology and Carcinogenesis Studies of 1-Trans-Delta9-Tetrahydrocannabinol
(CAS No. 1972-08-3) in F344 Rats and B6C3F1 Mice (Gavage Studies)", National
Toxicology Program, US Department of Health and Human Services, Nov
1996.

1996: "Marijuana smokers have the same cancer risks as
tobacco smokers, even though they may just smoke a
few joints a day." claims "Monitoring the Future Study", National Institute
of Drug Abuse, as reported by
planet-know.net.
(1)

1994: "Some forms of lung irritation may be more pronounced with chronic
marijuana smoke, but no signs of cancer were seen seven months after the
last dose" claims Dr William Slikker
Jr, researcher for a 2-1/2 year study of cannabis consumption by youth
for the National Center of Toxicological Research, Jefferson, AR.

1988: "As of October 1988, no case of lung cancer has ever been attributed
solely to marijuana use." claims Dr
Donald P Tashkin.

1987: "Whatever temporary changes marijuana may produce in the immune
system, they have not been found to increase the danger of infectious disease
or cancer. If there were significant damage, we might expect to find a higher
rate of these diseases among young people beginning in the 1960s, when marijuana
first became popular. There is no evidence of that." claims
Lester A Grinspoon, MD, "Marijuana",
The Harvard Medical School Mental Health Letter, Nov 1987, pg 3.

1985: "The result is that there is a four-fold greater burden of tar
on the lung from the smoke of a single marijuana joint compared to one
cigarette when each type is smoked the way it's ordinarily
smoked,' Tashkin said. Tashkin said he believes this poses a significant
cancer risk, although there is no direct evidence that pot smokers actually
suffer an unusually high incidence of lung cancer."  Associated Press
review of Dr Donald P Tashkin's
research published in New England Journal of Medicine.

1975: "Anticancer Activity of Cannabinoids", Journal of the National
Cancer Institute, Sept 1975.

" 'Controlling for age, sex, race, education,
alcohol consumption, pack-years of
cigarette smoking, and passive smoking, the risk of
squamous cell carcinoma of the head and neck was increased with marijuana
use. These associations were stronger for subjects who were 55 years of age
and younger.' claims Zuo-Feng Zhang, American Association for Cancer Research.
'If marijuana smoking has anything to do with smoking-related cancer, the
oral cavity would be the first site being affected,' he said. For the study,
performed while Zhang was working at New York's Memorial Sloan-Kettering
Cancer Center, researchers enrolled 173 patients with head or neck cancer
as well as a comparison group of 176 cancer-free blood donors of similar
age and sex. All study participants were questioned about their past use
of marijuana, tobacco and alcohol, workplace and
environmental exposure to possible carcinogens, and other aspects of their
background and lifestyle. Frequency of marijuana use was categorized as never,
less than or equal to once per day, and more than once per day. Duration
of use was categorized as never, one to five years and more than five years.
Among those who had ever used marijuana, the risk of head and neck cancer
was 2.6 times greater than among those who had never used the drug. (Researchers
arrived at this figure after adjusting for the effect of other risk factors,
such as smoking and alcohol.) They also observed a dose-response effect of
marijuana, with heavier users at higher cancer risk. Among people who reported
smoking marijuana once per day, the risk of head and neck cancer was 2.1
times that of someone who never used it, while among those who reported smoking
it more than once per day, the risk was 4.9 times that of those who had
abstained. Furthermore, people who were current smokers of both tobacco and
marijuana had by far the highest risk of head and neck cancer, indicating
that the two substances work together synergistically to promote cancer
development. Current users of both substances had 36 times the risk of head
and neck cancer found in people who used neither."
See another summary of the original 2004 article

Cannabidiol (CBD)

2013: "Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked.
In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by [the equivalent of] 40 percent during treatment.
... This is the first study, as far as we are aware, to demonstrate the impact of CBD on cigarette smoking. ...
These preliminary data, combined with the strong preclinical rationale for use of this compound,
suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration."
 "Cannabidiol reduces cigarette
consumption in tobacco smokers: Preliminary findings"
by Celia JA Morgan, Ravi K Das, Alyssa Joye, H Valerie Curran, Sunjeev K Kamboj,
Addictive Behaviors, vol 38 no 9, Sept 2013, pgs 2433-2436.

2010: "A combination of compounds in marijuana could help fight off
a particularly deadly form of braincancer, preliminary research suggests. Researchers
at the California Pacific Medical Center Research Institute (CPMCRI) combined
the non-psychoactive Cannabis compound, cannabidiol (CBD), with
9-tetrahyrdocannabinol (9-THC), the primary psychoactive
active ingredient in Cannabis. They found the combination boosts the inhibitory
effects of 9-THC on glioblastoma, the most common and aggressive form of
brain tumor. 'Our study not only suggests that combining these two compounds
creates a synergistic effect but it also helps identify molecular mechanisms
at work here, and that may lead to more effective treatments for glioblastoma
and potentially other aggressive cancers', said Sean McAllister, a scientist
at CPMCRI and the lead author of the study." 
"Marijuana
compounds may help fight brain cancer", Jan 16 2010

2006: "We investigated the anti-tumor activities of other plant
cannabinoids, i.e. cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid
and THC-acid, and assessed whether there is any advantage in using Cannabis
extracts (enriched in either cannabidiol or THC) over pure cannabinoids.
Results obtained in a panel of tumor cell lines clearly indicate that, of
the five natural compounds tested, cannabidiol is the most potent inhibitor
of cancer cell growth (IC50 between 6.0 and 10.6 µM), with
significantly lower potency in noncancer cells. The cannabidiol-rich extract
was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed
in the rank of potency. Both cannabidiol and the cannabidiol-rich extract
inhibited the growth of xenograft tumors obtained by subcutaneous injection
into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed
thyroid epithelial cells, and reduced lung metastases deriving from intra-paw
injection of MDA-MB-231 cells. Judging from several experiments on its possible
cellular and molecular mechanisms of action, we propose that cannabidiol
lacks a unique mode of action in the cell lines investigated. At least for
MDA-MB-231 cells, however, our experiments indicate that cannabidiol effect
is due to its capability of inducing apoptosis via: 1) direct or indirect
activation of cannabinoid CB2 [cannabinoid receptor type-2] and
vanilloid TRPV1 [transient receptor potential vanilloid type-1] receptors;
and 2) cannabinoid/vanilloid receptor-independent elevation of intracellular
Ca2+ and reactive oxygen species. Our data support the further
testing of cannabidiol and cannabidiol-rich extracts for the potential treatment
of cancer. ... In conclusion, our data indicate that cannabidiol, and possibly
Cannabis extracts enriched in this natural cannabinoid, represent a promising
non-psychoactive antineoplastic strategy. In particular, for a highly malignant
human breast carcinoma cell line we have shown here that cannabidiol and
a cannabidiol-rich extract counteract cell growth both in vivo and in vitro
as well as tumor metastasis in vivo. Cannabidiol exerts its effects on these
cells through a combination of mechanisms that include either direct or indirect
activation of CB2 and TRPV1 receptors, and induction of oxidative
stress, all contributing to induce apoptosis. Additional investigations are
required to understand the mechanism of the growth inhibitory action of
cannabidiol in the other cancer cell lines studied here." claim Alessia Ligresti,
Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti,
Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco,
Vincenzo Di Marzo,
"Anti-tumor
activity of plant cannabinoids with emphasis on the effect of cannabidiol
on human breast carcinoma", Endocannabinoid Research Group, Istituto
di Chimica Biomolecolare, CNR Pozzuoli, Italy, May 25 2006.

2005: "Health Canada's approval of Sativex was based on the results
of a four-week clinical trial involving 66 patients with MS-related neuropathic
pain that was carried out in Great Britain, in which half received Sativex
and the other half received a placebo. ... Sativex isolates the cannabinoid
components, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD),
representing only two of the more than 60 related chemicals that make up
the marijuana plant. It is believed that THC helps patients with pain while
CBD has a neurological effect, and that isolating these two cannabinoids
will enable patients to eliminate many of the side-effects that are associated
with the use of medical marijuana." reports David Hodges,
"Pot-based
drug shows promise for neuropathic pain", Medical Post vol 41
issue 19, May 17 2005.

2004: "Cannabis extracts may be well suited to treatment of inflammatory
diesases due to their multiple mechanisms of action. THC seemingly alleviates
pain, spasm and diarrhoea, while the CBD component presents the likelyhood
of immunomodulatory benefits. One recently demonstrated CBD effect is its
ability to inhibit TFN-a (tissue necrosis factor-alpha), a proven mechanism
of other agents employed to treat inflammatory bowel disease." reports
"Which
Conditions Are Treatable With Cannabis?", O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Spring 2004, citing
"The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic
therapeutic in murine collagen-induced arthritis." by AM Mafait, R Gallily,
PF Sumariwalla, AS Malik, E Andreakos, R Mechoulam, et al, Proceedings
of National Academy of Sciences USA 2000;97(17), pgs 9561-9566.

Cannabinoids

2006: "We investigated the anti-tumor activities of other plant
cannabinoids, i.e. cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid
and THC-acid, and assessed whether there is any advantage in using Cannabis
extracts (enriched in either cannabidiol or THC) over pure cannabinoids.
Results obtained in a panel of tumor cell lines clearly indicate that, of
the five natural compounds tested, cannabidiol is the most potent inhibitor
of cancer cell growth (IC50 between 6.0 and 10.6 µM), with
significantly lower potency in noncancer cells. The cannabidiol-rich extract
was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed
in the rank of potency. Both cannabidiol and the cannabidiol-rich extract
inhibited the growth of xenograft tumors obtained by subcutaneous injection
into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed
thyroid epithelial cells, and reduced lung metastases deriving from intra-paw
injection of MDA-MB-231 cells." claim Alessia Ligresti, Aniello Schiano Moriello,
Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis,
Chiara Laezza, Giuseppe Portella, Maurizio Bifulco, Vincenzo Di Marzo,
"Anti-tumor
activity of plant cannabinoids with emphasis on the effect of cannabidiol
on human breast carcinoma", Endocannabinoid Research Group, Istituto
di Chimica Biomolecolare, CNR Pozzuoli, Italy, May 25 2006.

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin,
cocaine, and the more common
alcohol and nicotine 
inhibit the growth of these new cells. It was thought that marijuana did
the same thing, but this new research suggests otherwise. ... The researchers
found that rats treated with HU-210 [a potent synthetic cannabinoid] on a
regular basis showed neurogenesis  the growth of new brain cells in
the hippocampus. A current hypothesis suggests depression may be triggered
when the hippocampus grows insufficient numbers of new brain cells. If true,
HU-210 could offer a treatment for such mood disorders by stimulating this
growth." reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2004: "The same family of chemicals that produces a buzz in marijuana
smokers may be responsible for 'runner's high,' the euphoric feeling that
some people get when they exercise, US researchers say. High levels of anandamide
were found in young men who ran or cycled at a moderate rate for about an
hour, according to a study made public this week by the Georgia Institute
of Technology and the University of California, Irvine. Anandamide is a
cannabinoid, or lipid molecule, that is naturally produced in the body. It
is known to produce sensations that are similar to those of THC, the psychoactive
property in marijuana." reports Reuters from
"Study
links marijuana buzz to 'runner's high' ", Jan 11 2004

"The 'endogenous' cannabinoid anandamide was shown to lower blood pressure
and heart rate through the CB1 receptor. The CB1 antagonist SR141716 was
shown to block the blood-pressure-lowering effects of anandamide. The researchers
guessed that the CB1 receptors were lowering blood pressure by vasodilation
through the sympathetic nervous system." claims Los Angeles Cannabis Resource
Center from
"Cannabinoids in
the Brain".

Cardiovascular

2005: "Eating low doses of THC, the active ingredient in cannabis,
helps prevent arteries clogging up, at least in mice. ... François
Mach at University Hospital in Geneva, Switzerland, wondered if this effect
might also help prevent the build-up of fatty deposits in arteries, or
atherosclerosis, by reducing the inflammation associated with this process.
Sure enough, when his team fed 1 milligram of THC per kilogram of bodyweight
- a low dose that should not have any psychotropic effects - to mice susceptible
to atherosclerosis, it greatly slowed the progress of the disease
(Nature, vol 434, p 782). The results are striking, says Michael Roth
of the University of California, Los Angeles, who wrote a commentary for
Nature. He stresses that the findings do not prove that smoking cannabis
will prevent atherosclerosis, pointing out that the mouse study suggests
the effect is dose-dependent and too little or too much THC has no protective
effect." 
"Cannabis
may help keep arteries clear", New Scintist, Apr 16 2005, pg 19.

2005: "Marijuana really does give you a headrush. In frequent cannabis
users, blood flows faster through the arteries of the brain than in people
who do not use the drug. ... Jean Cadet of the National Institute on Drug
Abuse ... measured blood flow in the brains of 54 frequent marijuana
smokers using a method called transcranial Doppler sonography. Even in the
group he describes as 'light' users, who smoked 11 joints a week on average,
there was a clear difference in blood flow compared with 18 controls. ...
(Neurology, vol 64, p 488)." 
"Marijuana
really does cause a headrush", New Scientist, Feb 12 2005, pg 17.

2005: "Smoking marijuana can affect blood flow in the brain so much
that it takes over a month to return to normal. And for heavy smokers, the
effects could last much longer, a new study suggests. Regular marijuana use
can harm memory and the ability to make decisions, according to Jean Cadet
at the National Institute on Drug Abuse in Baltimore, Maryland, US. To find
out why, he monitored the flow of blood through the brains of 54 marijuana
smokers, among whom the heaviest user smoked 50 joints every day. People
who smoked cannabis had higher blood flow through their brains than non-users.
Yet there was also greater resistance to the blood flow, suggesting that
cannabis changes the blood vessels in the brain in a way which hinders oxygen
in reaching the tissue effectively. In an attempt to compensate, extra blood
is sent to that part of the brain, increasing resistance but probably failing
to get enough oxygen through the vessels, Cadet suggests." 
"Marijuana makes
blood rush to the head", New Scientist, Feb 7 2005.

2005: "The active ingredient in cannabis protects arteries against
harmful changes that lead to strokes and heart attacks, new research suggests.
THC, or delta-9-tetrahydrocannabinol, is known to affect the brain and make
cannabis-users 'high'. The new research shows that it also has an influence
on blood vessels. A study of mice revealed that the compound blocks the process
of inflammation, which is largely responsible for the narrowing of arteries.
Inflammation combines with fatty deposits to produce obstructive 'plaques',
a condition known as atherosclerosis. These can block arteries to the heart,
causing angina and heart attacks, or to the brain, leading to strokes.
Atherosclerosis is the primary cause of heart disease and stroke in the Western
world, accounting for up to half the deaths from both conditions. The scientists,
led by François Mach, from Geneva University Hospital in Switzerland,
studied a strain of specially bred mice that are susceptible to narrowing
of the arteries. They were fed a high-cholesterol diet to make them develop
atherosclerotic plaques. Adding THC to their diet caused the growth of the
obstructions in their arteries to slow markedly after 11 months. When the
mice were given a chemical that blocked the action of THC, their arteries
continued to narrow at a fast rate." reports Nigel Hawkes, Times online,
Apr 7 2005.

2005: "The active ingredient of cannabis may protect against heart
disease and strokes ... If a similar effect can be demonstrated in people,
it would bring further ammunition to the camp of those who think that marijuana
(or rather its purified derivatives) should be treated seriously as a medicine.
Sadly for recreational users, though, the dose of THC required was very specific.
Too little or too much and the effect went away. Smoking spliffs is already
known to be bad for the heart. The protective effect Dr Steffens has demonstrated
is only limited compensation." claims Economist, Apr 7 2005.

2005: "Low doses of the main active ingredient in marijuana slowed
the progression of hardening of the arteries in mice, suggesting a hint for
developing a new therapy in people. ... The mouse work is presented
in Thursday's issue of the journal Nature by Dr. Francois Mach of
Geneva University Hospital in Geneva, Switzerland, and colleagues. ... Hardening
of the arteries sets the stage for heart attacks. Inflammation plays a key
role in the condition, characterized by a progressive buildup on the inside
walls of blood vessels. So Mach and colleagues explored the anti-inflammatory
effects of marijuana's main active ingredient, delta-9-tetrahydrocannabinol,
or THC. They fed mice a high-cholesterol diet for 11 weeks. About halfway
through that period, they started giving some of the mice very low, daily
oral doses of THC  too low to produce any marijuana-like changes in
behavior. At the end of the experiment, mice that had gotten the THC showed
less blood vessel clogging than did mice that got no THC. Related work showed
no additional benefit from higher THC doses, such as a person would get from
smoking marijuana, Mach noted. Researchers found that the benefit came from
THC's effect on immune-system cells. It reduced their secretion of an
inflammation-promoting substance and their migration to the vessel wall,
researchers found. It apparently did that by binding to proteins called CB2
receptors, which are found mostly on immune-system cells. THC also targets
CB1 receptors, found mostly in the brain. So the work suggests scientists
should try to develop a drug that works on CB2 receptors while ignoring the
brain receptors, Mach said." reports Malcolm Ritter, Associated Press, Apr
6 2005.

2002: "The neuroprotective effect of cannabinoids may have potential
clinical relevance for the treatment of neurodegenerative disorders such
as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson's
disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and
Patrick Weydt from
"Cannabis:
Old medicine with new promise for neurological disorders"

1982: "[there is no evidence that smoking marijuana] exerts a permanently
deleterious effect on the normal cardiovascular system." claims Institute
of Medicine.

"The 'endogenous' cannabinoid anandamide was shown to lower blood pressure
and heart rate through the CB1 receptor. The CB1 antagonist SR141716 was
shown to block the blood-pressure-lowering effects of anandamide. The researchers
guessed that the CB1 receptors were lowering blood pressure by vasodilation
through the sympathetic nervous system." claims Los Angeles Cannabis Resource
Center from
"Cannabinoids in
the Brain".

Cerebral Palsy

2000: "In August, Fayetteville police arrested Betty Wicker for marijuana
possession ... she was given three years probation. Although she told Judge
Storey the marijuana was used to fight debilitating cerebral palsy symptoms,
he said she would need to find another effective method to manage the condition.
Wicker, 42, shakes uncontrollably from head to foot, making simple conversation
difficult. Wicker said she was diagnosed with cerebral palsy in 1993, which
doctors believe could have been caused by a head injury she suffered when
falling from a horse as a teenager. When a Walnut Ridge doctor correctly
identified her condition, he said she had three options. Undergo brain surgery,
which could kill her, take 21 pills each day which could also kill her, or
smoke marijuana. In fact, Wicker said, the doctor specifically instructed
her to not stop smoking or she would wind up in a wheelchair within six months.
Yet due to the court ordered probation, Wicker is forced to take urinalysis
tests each week and to avoid legal trouble, she has discontinued smoking
marijuana ... 'My shaking gets really bad a lot of the time. I'm not taking
morphine shots, but I am back on morphine pills. I
would much rather smoke a little medical marijuana, but for now if I don't
take the morphine I would be unable to do anything.' " 
"Betty
Jean Wicker"

Cerebrovascular Ischemia

2002: "The neuroprotective effect of cannabinoids may have potential
clinical relevance for the treatment of neurodegenerative disorders such
as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson's
disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and
Patrick Weydt from
"Cannabis:
Old medicine with new promise for neurological disorders"

Chemotherapy

2005: "Controlled studies have revealed therapeutic utility of
cannabinoids in the treatment of ... cancer chemotherapy side-effects ...
THC itself is approved in the U.S. by the FDA, and it is used in many other
countries for the prevention of vomiting during cancer chemotherapy, and
for appetite enhancement. We, and many others, have found that not only THC
does that, but also the endocannabinoids. This is one of the main reasons
for high endocannabinoid levels during hunger and so on. Now, THC can be
used, and is being used, for these two things." claims
Dr Raphael Mechoulam, as reported
by David Jay Brown,
"The
New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael
Mechoulam".

1997: "A double-blind study confirmed that this synthetic drug [THC]
was preferred by chemotherapy patients by an almost two-to-one margin." claims
"Marijuana: Myths and Truth", Office of National Drug Control Policy. (No
explanation of what drug(s) THC was preferred to.)

1996: 80% of AIDS patients who had used cannabis preferred it to
prescription drugs including synthetic THC, claims B Wesner, "The Medical
Marijuana Issue Among PWAs: Reports of Therapeutic Use and Attitudes Toward
Legal Reform", Drug Research Unit, Social Science Research Institute, University
of Hawaii at Manoa.

1988: "Marijuana cigarettes in many cses are superior to synthetic
THC capsules in reducing chemotherapy-induced
nausea and vomiting. Marijuana cigarettes have an
important, clear advantage over synthetic THC capsules in that natural marijuana
is inhaled and generally takes effect more quickly than the synthetic capsule"
claims Francis L Young, Chief
Administrative Law Judge, US Drug Enforcement Administration, 1988.

1986: "I started feeling the changes pretty much right away. Smoking
marijuana also felt ten times better than taking Marinol
pill. It helped reduce my nausea and I could hold down
food better." claims Jim Kerns, cancer
and chemotherapy patient.

1983: "[Inhaled] Marijuana has been shown to be effective for many
cancer chemotherapy patients, safe dosage levels have been established and
a dosage regimen which minimizes undesirable side effects has been devised
and tested." claims California Research Advisory Panel, Annual Report
of the California Research Advisory Panel, vol 14, submitted to the Governor
and Legislature.

1981: "74 percent of the cancer patients treated in the program have
reported that [inhaled] marijuana is more effective in relieveing their nausea
and vomiting than any other drug they have tried." claims California Research
Advisory Panel, Annual Report of the California Research Advisory Panel,
vol 12, submitted to the Governor and Legislature.

"When our daughter was undergoing chemotherapy for lymph cancer, she was
sick and vomiting constantly as a result of her treatments. No legal drugs,
including Marinol, helped her. We finally turned to marijuana. With it, she
kept her food down, was comfortable and even gained weight. Those who say
Marinol and other drugs are satisfactory substitutes for marijuana may be
right in some cases but certainly not in all cases. If doctors can prescribe
morphine and other addictive medicines, it makes no sense to deny marijuana
to sick and dying patients when it can be provided on a carefully controlled,
prescription basis." claims Franklyn
"Lyn" Nofziger from his op-ed published in Washington Post, requoted
in "Medical
Marijuana: Reagan Aide Lyn Nofziger Dead at 81  Supported Patients'
Rights".

CNS

2003: "The major psychoactive constituent of Cannabis sativa,
delta(9)-tetrahydrocannabinol (delta(9)-THC), and endogenous cannabinoid
ligands, such as anandamide, signal through G-protein-coupled cannabinoid
receptors localised to regions of the brain associated with important
neurological processes. Signalling is mostly inhibitory and suggests a role
for cannabinoids as therapeutic agents in CNS disease where inhibition of
neurotransmitter release would be beneficial. ... This review highlights
recent advances in understanding of the endocannabinoid system and indicates
CNS disorders that may benefit from the therapeutic effects of cannabinoid
treatment." claims JL Croxford from
"Therapeutic
potential of cannabinoids in CNS disease", CNS Drugs 2003 #17(3),
pgs 179-202.

Colitis

"These [anti-inflammatory] drugs [Asacol,
Azulfidine, Pentasa,
Rowasa] provided minimal to no relief from symptoms
while causing kidney pain, burning urination, significant loss of hair, further
loss of appetite, and irritation to the rectum.... Using marijuana provided
great relief from the pain, cramping, and nausea. It also resulted in fewer
bowel movements each day, and increased my appetite helping me keep a more
stable body weight. I also noticed it improved my mood so I wasn't feeling
depressed all the time. In conjunction with marijuana I take hemp seed oil
which is also a powerful anti-inflammatory and has many other health benefits.
Using nothing but marijuana and hemp seed oil (no pharmaceutical drugs) I
was able to go from a very severe condition to complete remission and to
maintain it with out suffering any harsh side effects. If I stop using one
or the other for more than a few days I begin to develop symptoms ... I began
to research on the Internet and soon found many testimonials of other colitis
sufferers who also found relief in the use of marijuana. I also found many
articles containing scientific evidence that marijuana possesses
anti-inflammatory properties." claims anonymous Arkansas man from
"Patient Story
- Ulcerative Colitis".

2002: "Before she [Nofziger's daughter] died she underwent heavy
chemotherapy that caused nausea, diarrhea and loss of appetite. None of the
legal medications including the marijuana substitute Marinol helped to alleviate
the symptoms. In desperation, we turned to marijuana to see if that would
help. Fortunately, people know a lot more about where to find marijuana than
people of my generation. And the marijuana did help reduce the side effects
of the chemotherapy to the point where she regained her appetite and actually
began putting on weight. Obviously, it did not save her life nor did we think
it would. However, it made a portion of the last weeks of her life considerably
more bearable both to her and to her family. Since then I have learned that
marijuana can also help persons with glaucoma, the wasting symptoms of AIDS,
multiple sclerosis and other afflictions."  from
"Former
Reagan Aide Among Medical Marijuana Supporters" by Jim Burns, July 25
2002

1997: "A double-blind study confirmed that this synthetic drug [THC]
was preferred by chemotherapy patients by an almost two-to-one margin." claims
"Marijuana: Myths and Truth", US Office of National Drug Control Policy.
(No explanation of what drug(s) THC was preferred to.)

1996: 80% of AIDS patients who had used cannabis preferred it to
prescription drugs including synthetic THC, claims B Wesner, "The Medical
Marijuana Issue Among PWAs: Reports of Therapeutic Use and Attitudes Toward
Legal Reform", Drug Research Unit, Social Science Research Institute, University
of Hawaii at Manoa.

1981: "74 percent of the cancer patients treated in the program have
reported that [inhaled] marijuana is more effective in relieveing their nausea
and vomiting than any other drug they have tried." claims California Research
Advisory Panel, Annual Report of the California Research Advisory Panel,
vol 12, submitted to the Governor and Legislature.

"When our daughter was undergoing chemotherapy for lymph cancer, she was
sick and vomiting constantly as a result of her treatments. No legal drugs,
including Marinol, helped her. We finally turned to marijuana. With it, she
kept her food down, was comfortable and even gained weight. Those who say
Marinol and other drugs are satisfactory substitutes for marijuana may be
right in some cases but certainly not in all cases." claims
Franklyn "Lyn" Nofziger from
his op-ed published in Washington Post, requoted in
"Medical
Marijuana: Reagan Aide Lyn Nofziger Dead at 81  Supported Patients'
Rights".

"I have Multiple Sclerosis and have been able to receive little to no relief
from the FDA approved medicines my doctors recommended. The doctors had me
on Ritalin to give me energy and Prozac to keep my moods level. I took Vicodin
[hydrocodone and
acetaminophen] and Soma to help with pain. I
had to learn to give myself shots, so that I could take my Copaxone drug
... I am not taking any of those drugs now, I haven't for four years now
I have been smoking medical marijuana. Since I have been medicating my body
with marijuana I have never felt better, my disease has mostly gone into
remission ... I am able to work part time and that was not something that
was thought possible four short years ago. Marijuana has changed my life
with the best possible thing - Hope." claims Meagan Boyd from
"Patient
Testimonials".

2006: "... a normally healthy 70-kilogram (154-pound) adult can achieve
a relaxed affability from approximately 33 grams of ethyl
alcohol. This effective dose can come from two 12-ounce
beers, two 5-ounce glasses of wine or two 1.5-ounce shots of 80-proof vodka.
The median lethal dose for such an adult is approximately 330 grams, the
quantity contained in about 20 shots of vodka. A person who consumes that
much (10 times the median effective dose), taken within a few minutes on
an empty stomach, risks a lethal reaction. ... The most toxic recreational
drugs, such as GHB (gamma-hydroxybutyrate) and
heroin, have a lethal dose less than 10 times their
typical effective dose. The largest cluster of substances has a lethal dose
that is 10 to 20 times the effective dose: These include
cocaine, MDMA
(methylenedioxymethamphetamine, often called "ecstasy")
and alcohol. A less toxic group of substances, requiring 20 to 80 times the
effective dose to cause death, include Rohypnol
(flunitrazepam or "roofies") and
mescaline (peyote cactus). The least physiologically
toxic substances, those requiring 100 to 1,000 times the effective dose to
cause death, include psilocybin mushrooms and
marijuana, when ingested. I've found no published cases in the English language
that document deaths from smoked marijuana, so the actual lethal dose is
a mystery. My surmise is that smoking marijuana is more risky than eating
it but still safer than getting drunk. ... statistics show that every year
about 300 people die in the United States from an alcohol overdose, and for
at least twice that number of overdose deaths, alcohol is considered a
contributing cause." claims Robert S
Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006. Also see chart
"Ranking
psychoactive substances  ratio of fatal dose to effective dose"

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin,
cocaine, and the more common
alcohol and nicotine 
inhibit the growth of these new cells. It was thought that marijuana did
the same thing, but this new research suggests otherwise. ... The researchers
found that rats treated with HU-210 [a potent synthetic cannabinoid] on a
regular basis showed neurogenesis  the growth of new brain cells in
the hippocampus. " reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2004: "Marijuana is a dangerous drug, a surprisingly dangerous drug.
More teenagers are treated for marijuana abuse than for abuse of any other
substance, including alcohol, and any law making marijuana
more accessible will exacerbate the problem." claims Tom Riley, spokesperson
for US Office of National Drug Control Policy, from "Medical Marijuana Use
Gains Support" by Bill Broadway, Detroit News, July 4 2004.

2000: "... some drugs have a Safety Ratio or Therapeutic Index of
just 10:1 or 20:1 or so (while some chemo therapy drugs only have a 'safety'
ratio of about 1.5:1!) Alcohol's Safety Ratio is as
low as ~ 4:1. So, if you drink about 4 times as much as you 'need' you may
well kill yourself. On the other hand, THC, which is sometimes considered
the 'most toxic' component in Cannabis (by some people) has a Safety Ratio
or Therapeutic Index that is much higher than 40,000:1. [The T.I. or S.I.
tells you how many normal doses of something you can take before you reach
the LD-50% level for this material.] [LD-50% = Lethal Dose for 50% of the
test subjects for a given substance.]" claims Pat from
"Cannabis vs
Dilantin. Safety Ratio. WoDs, etc.", Marihemp, July 2 2000.

1997: "Fact: No credible medical research has shown smoked marijuana
to be safe, effective, or therapeutically superior to other substances that
have fewer side effects." claims "Marijuana: Myths and Truth", US Office
of National Drug Control Policy. (see
Patients
Out of Time's Rebuttal)

1995: "The smoking of cannabis, even long term, is not harmful to
health." claims the British scientific journal Lancet.

1988: "In strict medical terms marijuana is far safer than many foods
we commonly consume. For example, eating 10 raw potatoes can result in a
toxic response. By comparison, it is physically impossible to eat enough
marijuana to induce death. Marijuana in its natural form is one of the safest
therapeutically active substances known to man. By any measure of rational
analysis marijuana can be safely used within the supervised routine of medical
care." claims Drug Enforcement Administration's Chief Administrative Law
Judge Francis L Young, "In the Matter
of Marijuana Rescheduling Petition," [Docket #86-22], Sept 6, 1988, pg 57.

1978: "Federally funded studies of long-tern users of high-potency
marijuana in three foreign countries showed no difference between the health,
ability to work, and brain function of users and non-users, a number of
researchers said ... Studies showed little if any harm from the marijuana
smoking. [Dr Max] Fink [of the department of psychiatry of the State University
of New York at Stony Brook] called the poisonous effects of marijuana, as
shown in the studies, 'trivial at best.' ... A team of Greek doctors, giving
physicals to 60 marijuana users compared to 64 nonusers, also found no difference
in the health of the two groups." reports Stuart Auerbach in "Studies See
No Health Effect of Pot Smoking, Researchers Say", Washington Post, Jan 28
1978.

1972: "A careful search of the literature and testimony of the nation's
health officials has not revealed a single human fatality in the United States
proven to have resulted solely from ingestion of marihuana. Experiments with
the drug in monkeys demonstrated that the dose required for overdose death
was enormous and for all practical purposes unachievable by humans smoking
marihuana. This is in marked contrast to other substances in common use,
most notably alcohol and barbiturate sleeping pills."
claims Raymond P Shafer, et al,
Marihuana:
A Signal of Misunderstanding, National Commission on Marihuana and
Drug Abuse.

2004: "17,000 people died from Tylenol toxicity the last year they
have data. So, I mean the reality is, if you look at it rationally, Tylenol
is a very dangerous drug; its un-regulated, over-the-counter." claims
Dr Joel Hochman, Founder & Exec Dir, National Foundation for the Treament
of Pain,
Cultural
Baggage radio show, Aug 10 2004.

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and acetaminophen] 1 or 2 per day
for severe headaches, Marinol to provide some daily control and
Doxipin [dibenzoxepin] and
Lithium to control the depression associated
with his constant turmoil. ... Having seen him in constant pain without the
availability of the Marinol or marijuana purchased from a street dealer,
I have no question that there is pain relief afforded to him by the drug.
It should be noted that the Marinol only gives him partial and inadequate
pain relief." claims Dr Michael E Mayle, DO, in a letter to Whom It May Concern,
1996.

"I have Multiple Sclerosis and have been able to receive little to no relief
from the FDA approved medicines my doctors recommended. ... I took Vicodin
[hydrocodone and acetaminophen] and Soma to help with
pain. ... I am not taking any of those drugs now, I haven't for four years
now I have been smoking medical marijuana. Since I have been medicating my
body with marijuana I have never felt better, my disease has mostly gone
into remission ... I am able to work part time and that was not something
that was thought possible four short years ago. Marijuana has changed my
life with the best possible thing - Hope." claims Meagan Boyd from
"Patient
Testimonials".

"The nerves in my neck were smashed in a gunshot accident ... I can move
my arm, but I can't move my fingers. There is a kind of numbness from my
left shoulder down to my pinkie. But there is also a burning feeling, like
needles. I can't stand for anything to touch my arm  if I accidently
hit it there is extreme pain. It throbs 24 hrs a day. I've been on numerous
strong medicines, including Tawan NX, Vicodin 10 mg
[hydrocodone and acetaminophen] , and
methadone 10 mg 4 to 5 pills per day. Some days I
can take less, depending on how much I use marijuana. I don't smoke to get
stoned, I smoke it for relief from thinking about my arm all the time and
to take away the pain. When I smoke marijuana, I can get things done around
the house, it gets me energetic, gives me an appetite. I don't have an appetite
when I don't have marijuana  I have to force myself to eat. The narcotics
give you a state of mind where you don't eat  I had to get off Vicodin
 I was taking too much  it was hurting my kidneys. There's some
kind of aspirin in it, 600 mg per tablet, 5-6 tablets per day  we caught
it just in time before it ruined my kidneys. So they put me back on methadone
 I didn't want to get back on that  it makes me nauseated, not
eat, sometimes makes me depressed. When I smoke, I don't have to take very
much methadone and I have a better outlook on life." claims anonymous patient
from
"Nerve
Damage".

"I have hypoglycemia, a form of diabetes. ... The second condition I treat
with marijuana is TMJ disorder, referring to the temporo-mandibular joint
of the jaw. Over the years, this condition has worn my cartilage away. The
severity of pain is hard to describe, but if the pain was ranked in levels
up to 5, I would say that level 3 I am nauseated from the pain. At level
4 I can barely move my jaws enough to talk and eating is difficult. The real
challenge is to not vomit from the pain, because vomiting flexes my jaw.
At level 5, I can't avoid vomiting and I can't eat, which causes my blood
sugar to drop dangerously low. ... For the pain, I've tried Vicodin
[hydrocodone and acetaminophen] , but marijuana is
as effective as two Vicodin and the relief is immediate with easily controlled
dosage. For the nausea and vomiting, marijuana is amazing. The nausea stops
in two minutes, period. Even if I'm already vomiting, I can still get it
in my system with a few puffs. ... I've been on Vicodin since December 2001,
which is a very addicting drug and not recommended for long term use. Not
only am I having symptoms of physical addiction, but it's making my condition
worse by staying in my system too long and putting me into deep sleep which
causes my blood sugar to drop. So the episodes that normally last 4-5 days
are now lasting two weeks or more. When it finally eases up, I go through
withdrawal. ... I believe God put marijuana on Earth as medicine to help
people. I don't believe opiate addiction is part of God's plan for me. I
could leave my home and family for a state where medical marijuana laws would
protect me, but I am a grandmother and a granddaughter and don't want to
leave my loved ones. ... Our doctor would recommend marijuana if he didn't
face the threat of losing his license." claims anonymous female patient from
"Appetite
and Pain".

2008: "... the relative risk of ... contracting head and neck
cancer in marijuana users was the same (1.0)
as in those who had never smoked cannabis. These results differ from the
relative risk of contracting cancer from ... heavy consumption of alcohol
(5.7), compared with those who abstained from those activities." 
"Small
study shows marijuana does not increase risk of head, neck cancer", Mar
5 2008

2006: "... a normally healthy 70-kilogram (154-pound) adult can achieve
a relaxed affability from approximately 33 grams of ethyl alcohol. This effective
dose can come from two 12-ounce beers, two 5-ounce glasses of wine or two
1.5-ounce shots of 80-proof vodka. The median lethal dose for such an adult
is approximately 330 grams, the quantity contained in about 20 shots of vodka.
A person who consumes that much (10 times the median effective dose), taken
within a few minutes on an empty stomach, risks a lethal reaction. ... The
largest cluster of substances has a lethal dose that is 10 to 20 times the
effective dose: These include cocaine, MDMA
(methylenedioxymethamphetamine, often called "ecstasy")
and alcohol. ... My surmise is that smoking marijuana is more risky than
eating it but still safer than getting drunk. ... statistics show that every
year about 300 people die in the United States from an alcohol overdose,
and for at least twice that number of overdose deaths, alcohol is considered
a contributing cause." claims Robert
S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006.

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin,
cocaine, and the more common alcohol and
nicotine  inhibit the growth of these new cells.
It was thought that marijuana did the same thing, but this new research suggests
otherwise. ... The researchers found that rats treated with HU-210 [a potent
synthetic cannabinoid] on a regular basis showed neurogenesis  the
growth of new brain cells in the hippocampus. " reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2003: "Smoking marijuana ... does not cause permanent
brain damage, researchers from the University of California
at San Diego said Friday in a study. ... Other illegal drugs, or even alcohol,
can cause brain damage. ..." reports
Walter Cronkite,
"Pot Doesn't
Harm Brain, Study Shows", June 30 2003

2003: "Women who used marijuana also had a lower risk of total mortality
as compared to those who consumed alcohol regularly. from
"Marijuana
Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Jouurnal
of the California Cannabis Research Medical Group, Summer 2003.

1996: "Compared to alcohol, which makes people take more risks on
the road, marijuana made drivers slow down and drive more carefully.... Cannabis
is good for driving skills, as people tend to overcompensate for a perceived
impairment." claims Professor Olaf Drummer, a forensic scientist the Royal
College of Surgeons in Melbourne, Australia.

1989: "No evidence for a Role of Alcohol or Other Psychoactive Drugs
in Accelerating Immunodeficiency in HIV-1 Positive Individuals", Multicenter
AIDS Cohort Study, Journal of the American Medical Association, June
16, 1989.

1968: "The evidence of a link with violent crime is far stronger with
alcohol than with the smoking of cannabis." claims British Advisory Committee
on Drug Dependence in The Wooten Report: Committee on Drug Dependence,
Cannabis

1988: "My family obtained some marijuana for me and I began to use
it along with Xanax ... the marijuana put me at cruising speed, regulated
and even. Eventually I was able to reduce my use of Xanax ..." claims Karen
Ross, from Marihuana, The Forbidden Medicine, by
Lester A Grinspoon &
James B Bakalar, Yale University
Press, New Haven, CT, pg 102.

1988: "My family obtained some marijuana for me and I began to use
it along with Xanax and Elavil ... the marijuana put me at cruising speed,
regulated and even. Eventually I was able to reduce my use of Xanax and stop
using Elavil entirely." claims Karen Ross, from Marihuana, The Forbidden
Medicine, by Lester A Grinspoon
& James B Bakalar, Yale University
Press, New Haven, CT, pg 102.

2004: "... she was able to control her seizures with ... Tegretol.
About 5 years ago she started having auras and seizures that no prescription
medication was able to control. ... The reason I'm writing is because we
know that cannabis (marijuana) prevents her seizures. Not only do I know
this but there are thousands of other patients out there that know it." claims
"phatboy" 
"5000
year old drug prevents seizures.", Epilepsy Foundation eCommunities Forums,
Jan 8 2004.

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin, cocaine,
and the more common alcohol and
nicotine  inhibit the growth of these new cells.
It was thought that marijuana did the same thing, but this new research suggests
otherwise. ... The researchers found that rats treated with HU-210 [a potent
synthetic cannabinoid] on a regular basis showed neurogenesis  the
growth of new brain cells in the hippocampus. " reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and
acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium to control the depression
associated with his constant turmoil. ... The only drug that seems to
give William any true relief from pain is that from smoking marijuana. ...
Having seen him in constant pain without the availability of the Marinol
or marijuana purchased from a street dealer, I have no question that there
is pain relief afforded to him by the drug. It should be noted that the Marinol
only gives him partial and inadequate pain relief." claims Dr Michael E Mayle,
DO, in a letter to Whom It May Concern, 1996.

"... a chronic fatigue/fibromyalgia support group recommended marijuana ...
for [my] post polio syndrome. I was amazed. Just a few puffs took away the
pain. I was able to move around comfortably to walk, clean my house, and
do all the things I needed to do. While living in California, and then for
awhile in Hawaii, I had legal access to marijuana. This was during the time
after these states had made marijuana available for medical use. ... I returned
to Arkansas ... Since my return, I have not been able to obtain marijuana.
My doctor has prescribed a variety of medications but these seem to have
little effect on my symptoms. I still feel stiff and my body aches. The worst
part is that these drugs make me very groggy. I'm afraid to drive and I don't
feel very sociable. ... I don't know how much these powerful pain medications
may be contributing to my depression, but now I'm also having to take strong
mood altering drugs to control the depression. I take Darvocet for pain,
Flexeril for muscle spasms, Doxipin [dibenzoxepin] for pain and as a sedative,
Celexa for depression, and Klonopin as an antidepressant. ... I am seriously
considering moving to one of the states where marijuana is available ..."
claims Jean Cooper from
"Patient
Story - Jean - Childhood Polio".

2006: "A less toxic group of substances, requiring 20 to 80 times
the effective dose to cause death, include Rohypnol (flunitrazepam or "roofies")
and mescaline (peyote cactus). The least physiologically
toxic substances, those requiring 100 to 1,000 times the effective dose to
cause death, include psilocybin mushrooms and
marijuana, when ingested. I've found no published cases in the English language
that document deaths from smoked marijuana, so the actual lethal dose is
a mystery." claims Robert S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006

2006: "The most toxic recreational drugs, such as GHB
(gamma-hydroxybutyrate) and heroin, have a lethal
dose less than 10 times their typical effective dose. ... The least
physiologically toxic substances, those requiring 100 to 1,000 times the
effective dose to cause death, include psilocybin
mushrooms and marijuana, when ingested. I've found no published cases in
the English language that document deaths from smoked marijuana, so the actual
lethal dose is a mystery." claims Robert
S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006.

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and
acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium to control the
depression associated with his constant turmoil. ... The only drug
that seems to give William any true relief from pain is that from smoking
marijuana. ... Having seen him in constant pain without the availability
of the Marinol or marijuana purchased from a street dealer, I have no question
that there is pain relief afforded to him by the drug." claims Dr Michael
E Mayle, DO, in a letter to Whom It May Concern, 1996.

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ...
My neurologist prescribed the drugs Compazine and Antivert. They had little
affect on the nausea and no affect on the appetite, even after the dosage
was doubled. After a couple of weeks of feeling sick and not eating, I had
lost 15 pounds and no medication was helping. ... I decided to try smoking
Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke
were gone I began to relax and get an appetite. I could finally eat again.
Since that time, I have used cannabis to maintain a healthy body weight and
a decent standard of living. For years I left my prescription drugs setting
on the counter, as Cannabis was more effective." cliams John E Precup from
"Patient
Testimonials"

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... There are occasions when he is
seen in the office or the emergency room and given shots of Demerol [meperidine]
and Phenergren [promethazine]. Even these shots do not give him full relief
of his headaches, but do, when things are severe, give him a few hours
of peace. The only drug that seems to give William any true felief from
pain is that from smoking marijuana. ... Having seen him in constant pain
without the availability of the Marinol or marijuana purchased from a street
dealer, I have no question that there is pain relief afforded to him by the
drug. It should be noted that the Marinol only gives him partial and inadequate
pain relief." claims Dr Michael E Mayle, DO, in a letter to Whom It May Concern,
1996.

2005: "Cannabis-using Crohn's patients ... are
also able to reduce the amount of immunosuppressive medications that have
been a mainstay of conventional treatment. ... Asacol and Pentasa brands
of Mesalamine, an anti-inflammatory medication with immuno-modulating
properties is also reduced in many cases. ... Mesalamine frequently was reported
to cause rash, itching, and photosensitivity." reports Jeff Hergenrather,
"Cannabis Alleviates
Symptoms of Chrohn's [sic] Disease", O'Shaughnessy's Journal of the
California Cannabis Research Medical Group, Autumn 2005.

2005: "I've managed a Crohn's affliction very well for 20 years, the
last 12 of them prescription free except for one month when upon getting
a colonoscopy and being willing to try something else, I agreed to try Pentasa.
I pooped my brains out almost immediately and for the next 5 days in spite
of taking the drug for only two, on the maximum dose the doctor felt I needed.
I had to work up to that dose slowly after two weeks off of it, and it seemed
to work ..." claims James Moore,
Crohn's patient.

"These [anti-inflammatory] drugs [Asacol, Azulfidine, Pentasa, Rowasa] provided
minimal to no relief from symptoms while causing kidney pain, burning urination,
significant loss of hair, further loss of appetite, and irritation to the
rectum.... Using marijuana provided great relief from the pain, cramping,
and nausea. It also resulted in fewer bowel movements each day, and increased
my appetite helping me keep a more stable body weight. I also noticed it
improved my mood so I wasn't feeling depressed all the time." claims anonymous
Arkansas man from
"Patient Story
- Ulcerative Colitis".

2006: "A less toxic group of substances, requiring 20 to 80 times
the effective dose to cause death, include Rohypnol
(flunitrazepam or "roofies") and mescaline (peyote
cactus). The least physiologically toxic substances, those requiring 100
to 1,000 times the effective dose to cause death, include
psilocybin mushrooms and marijuana, when ingested.
I've found no published cases in the English language that document deaths
from smoked marijuana, so the actual lethal dose is a mystery." claims
Robert S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006.

2006: "The largest cluster of substances has a lethal dose that is
10 to 20 times the effective dose: These include
cocaine, MDMA (methylenedioxymethamphetamine, often
called "ecstasy") and alcohol. ... The least
physiologically toxic substances, those requiring 100 to 1,000 times the
effective dose to cause death, include psilocybin
mushrooms and marijuana, when ingested. I've found no published cases in
the English language that document deaths from smoked marijuana, so the actual
lethal dose is a mystery." claims Robert
S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006.

1999: "In 1992 I was found to have testicular cancer. My chemotherapy
put me in the hospital for five days at a time, once a month, for four months.
But midway through my treatment I could tell that Zofran, then a hot new
drug prescribed to combat nausea, was losing its effect. For the remainder
of my chemotherapy I turned to marijuana to keep my head out of the toilet.
None of the doctors or nurses at the hospitals I went to for treatment (New
York University Medical Center) or consultation (Memorial Sloan-Kettering)
discouraged me from using marijuana should the need arise. They said they
had patients who had benefited from it when other drugs had failed." claims
Richard Brookhiser, senior
editor of National Review, from a letter to New York Times,
May 22, 1999.

2006: "... National Survey on Drug Use and Health, conducted in 2004,
counted about 97 million Americans who have tried marijuana, compared to
3 million who have tried heroin (166,000 had used it in the previous month).
That's not much of a rush through the gateway.
And a number of studies have demonstrated that your chances of becoming an
addict are higher if addiction runs in your family, or if heroin is readily
available in your community, or if you're a risk-taker. These factors can
account for the total number of heroin addicts, which could make the gateway
theory superfluous. On close inspection, [Mount Sinai School of Medicine
Prof Yasmin] Hurd's research, published in the journal
Neuropsychopharmacology,
doesn't show otherwise. For the most part, it's a blow to the gateway theory.
To be sure, Hurd found that rats who got high on pot as adolescents used
more heroin once they were addicted. But she found no evidence that they
were more likely to become addicted than the rats in the control group who'd
never been exposed to delta-9-tetrahydrocannabinol, or THC, marijuana's main
ingredient. ... The control rats paced their cages and repeatedly pressed
the active bars even when the light indicating availability wasn't on. The
pot rats, on the other hand, figured out that the heroin was available only
at certain times, and that pacing and tapping the bar incessantly wasn't
worth the trouble. When heroin was available, the marijuana rats took more
of it. But when it wasn't, they chilled in the corner." reports Ryan Grim,
"Gateway to Nowhere? The evidence
that pot doesn't lead to heroin.",
Slate, July 20 2006.

2006: "The most toxic recreational drugs, such as GHB
(gamma-hydroxybutyrate) and heroin, have a lethal dose
less than 10 times their typical effective dose. ... The least physiologically
toxic substances, those requiring 100 to 1,000 times the effective dose to
cause death, include psilocybin mushrooms and
marijuana, when ingested. I've found no published cases in the English language
that document deaths from smoked marijuana, so the actual lethal dose is
a mystery." claims Robert S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006.

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin,
cocaine, and the more common
alcohol and nicotine 
inhibit the growth of these new cells. It was thought that marijuana did
the same thing, but this new research suggests otherwise. ... The researchers
found that rats treated with HU-210 [a potent synthetic cannabinoid] on a
regular basis showed neurogenesis  the growth of new brain cells in
the hippocampus. " reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2004: "Well, the drug war has, from a physicians point of view;
the drug war has become a war on doctors who dare to competently and adequately
treat pain. The data now is that probably, at the wildest estimate, there
may 30 to 40 thousand doctors out of the million doctors in the United States
who hold a narcotics license, there may be 30 or 40 thousand who are willing
to effectively treat pain management provide pain management. And in
2002 about 600 of them were prosecuted by the DEA which gives you a ratio
of about one out every 80 practicing, full-time pain management doctors became
a victim of the war on doctors and since the rate of incidence is cumulative,
if you add another 600 in 2003, thats about 1,000 to 1,200 doctors
have gone through a career shattering experiences out of perhaps 40,000,
so thats one out every 40 practicing pain management doctors has gone
through this. So its an outrageous situation and its no wonder
that very few doctors are willing to treat patients in pain ... Its
all because of the mythology of the addiction from opioids, that if you take
opioid medication youre inevitably going to become addicted, which
is complete mythology. Ive even had patients tell me that doctors have
told them, 'You cant take these medicines because it will destroy your
brain, it will destroy your liver.' When the truth of this matter is that
these medicines are among the safest medicines prescribed in medicine today
and in contrast well, for example, theres not one documented case
of a patient dying from an overdose of oxycotin when they took the medicine
as prescribed by their physician. In contrast, 17,000 people died from
Tylenol toxicity the last year they have data.
So, I mean the reality is, if you look at it rationally, Tylenol is a very
dangerous drug; its un-regulated, over-the-counter. Opioids, which
are extremely safe medications when taken as prescribed, and very effective,
life-saving for an intractable pain patient, these are the focus of a campaign
to absolutely discourage physicians from prescribing them." claims Dr Joel
Hochman, Founder & Exec Dir, National Foundation for the Treament of
Pain,
Cultural
Baggage radio show, Aug 10 2004.

2004: "The Emmy award-winning host [Montel Williams] of the nationally
syndicated Montel Williams Show, recalled how prescription painkillers
and even morphine failed to control his tremors and spasms. Williams said
it was not until he started using marijuana that he was able to feel like
a 'contributing member of society.' " reports Alicia Chang from
"Montel
Williams Pushes Pot  for Medical Relief", Associated Press, May
4 2004.

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox [oxycodone
and acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium
to control the depression associated with his constant turmoil. ...
Having seen him in constant pain without the availability of the Marinol
or marijuana purchased from a street dealer, I have no question that there
is pain relief afforded to him by the drug." claims Dr Michael E Mayle, DO,
in a letter to Whom It May Concern, 1996.

"I have Multiple Sclerosis and have been able to receive little to no relief
from the FDA approved medicines my doctors recommended. ... I took Vicodin
[hydrocodone and acetaminophen] and Soma to
help with pain. ... I am not taking any of those drugs now, I haven't for
four years now I have been smoking medical marijuana. Since I have been
medicating my body with marijuana I have never felt better, my disease has
mostly gone into remission ... I am able to work part time and that was not
something that was thought possible four short years ago. Marijuana has changed
my life with the best possible thing - Hope." claims Meagan Boyd from
"Patient
Testimonials".

"The nerves in my neck were smashed in a gunshot accident ... I can move
my arm, but I can't move my fingers. There is a kind of numbness from my
left shoulder down to my pinkie. But there is also a burning feeling, like
needles. I can't stand for anything to touch my arm  if I accidently
hit it there is extreme pain. It throbs 24 hrs a day. I've been on numerous
strong medicines, including Tawan NX, Vicodin 10 mg [hydrocodone and
acetaminophen] , and methadone 10 mg 4 to 5
pills per day. Some days I can take less, depending on how much I use marijuana.
I don't smoke to get stoned, I smoke it for relief from thinking about my
arm all the time and to take away the pain. When I smoke marijuana, I can
get things done around the house, it gets me energetic, gives me an appetite.
I don't have an appetite when I don't have marijuana  I have to force
myself to eat. The narcotics give you a state of mind where you don't eat
 I had to get off Vicodin  I was taking too much  it was
hurting my kidneys. There's some kind of aspirin in it, 600 mg per tablet,
5-6 tablets per day  we caught it just in time before it ruined my
kidneys. So they put me back on methadone  I didn't want to get back
on that  it makes me nauseated, not eat, sometimes makes me depressed.
When I smoke, I don't have to take very much methadone and I have a better
outlook on life." claims anonymous patient from
"Nerve
Damage".

"I have hypoglycemia, a form of diabetes. ... The second condition I treat
with marijuana is TMJ disorder, referring to the temporo-mandibular joint
of the jaw. Over the years, this condition has worn my cartilage away. The
severity of pain is hard to describe, but if the pain was ranked in levels
up to 5, I would say that level 3 I am nauseated from the pain. At level
4 I can barely move my jaws enough to talk and eating is difficult. The real
challenge is to not vomit from the pain, because vomiting flexes my jaw.
At level 5, I can't avoid vomiting and I can't eat, which causes my blood
sugar to drop dangerously low. ... For the pain, I've tried Vicodin [hydrocodone
and acetaminophen] , but marijuana is as effective
as two Vicodin and the relief is immediate with easily controlled dosage.
For the nausea and vomiting, marijuana is amazing. The nausea stops in two
minutes, period. Even if I'm already vomiting, I can still get it in my system
with a few puffs. ... I've been on Vicodin since December 2001, which is
a very addicting drug and not recommended for long term use. Not only am
I having symptoms of physical addiction, but it's making my condition worse
by staying in my system too long and putting me into deep sleep which causes
my blood sugar to drop. So the episodes that normally last 4-5 days are now
lasting two weeks or more. When it finally eases up, I go through withdrawal.
... I believe God put marijuana on Earth as medicine to help people. I don't
believe opiate addiction is part of God's plan for me. I could leave my home
and family for a state where medical marijuana laws would protect me, but
I am a grandmother and a granddaughter and don't want to leave my loved ones.
... Our doctor would recommend marijuana if he didn't face the threat of
losing his license." claims anonymous female patient from
"Appetite
and Pain".

2001: "I have smoked weed off and on for 20 years, and now everyday.
I find that with it I take less Paxil, and I am able to function better.",
Manic-depression/obsessive compulsive disorder patient, Mar 11 2001.

"People being treated with Paxil have become violent and suicidal. Others
have complained of severe withdrawal reactions." claims Law Offices of James
Sokolove.
paxil-side-effects-lawsuits.com

2004: "Most of her life she was able to control her seizures with
... Phenobarbital ... About 5 years ago she started having auras and seizures
that no prescription medication was able to control. ... The reason I'm writing
is because we know that cannabis (marijuana) prevents her seizures. Not only
do I know this but there are thousands of other patients out there that know
it." claims "phatboy" 
"5000
year old drug prevents seizures.", Epilepsy Foundation eCommunities Forums,
Jan 8 2004.

2003: "DeLorenzo and his colleagues in the VCU Department of Neurology
and the Department of Pharmacology and Toxicology ... injected chronically
epileptic rats with different combinations of six drugs: 1) an extract of
marijuana, 2) two synthetic drugs that include the key psychoactive ingredients
in marijuana, 3) the common anticonvulsant drugs Phenobarbital and phenytoin
and 4) a drug to block the activation of the CB1 receptor by cannabinoids
in the brain. The marijuana extract and synthetic marijuana drugs completely
eliminated the rats seizures, which averaged three over a 10-hour period.
The Phenobarbital ...failed to completely eliminate the seizures." claims
Robert J DeLorenzo from
"Marijuana
and its receptor protein in brain control epilepsy", VCU News, Sept 30
2003.

2004: "Most of her life she was able to control her seizures with
dilantin ... About 5 years ago she started having auras and seizures that
no prescription medication was able to control. ... The reason I'm writing
is because we know that cannabis (marijuana) prevents her seizures. Not only
do I know this but there are thousands of other patients out there that know
it." claims "phatboy" 
"5000
year old drug prevents seizures.", Epilepsy Foundation eCommunities Forums,
Jan 8 2004.

2003: "DeLorenzo and his colleagues in the VCU Department of Neurology
and the Department of Pharmacology and Toxicology ... injected chronically
epileptic rats with different combinations of six drugs: 1) an extract of
marijuana, 2) two synthetic drugs that include the key psychoactive ingredients
in marijuana, 3) the common anticonvulsant drugs Phenobarbital and phenytoin
and 4) a drug to block the activation of the CB1 receptor by cannabinoids
in the brain. The marijuana extract and synthetic marijuana drugs completely
eliminated the rats seizures, which averaged three over a 10-hour period.
The ... phenytoin failed to completely eliminate the seizures." claims Robert
J DeLorenzo from
"Marijuana
and its receptor protein in brain control epilepsy", VCU News, Sept 30
2003.

2000: "I've heard that Dilantin is ~ the World's best anti-seizure
drug and that it can be a very effective, fast-acting anti-depressant. Also,
as I recall, one animal study was done with Dilantin and it ~ significantly
extended the average lifespan of the animals. ... the full suite of Cannabinoids
from the Cannabis Plant perform together as the World's most effective
anti-seizure 'agent' or combination. Also, this herbal extract blend of
Cannabinoids is a very safe and effective anti-depressant medicine ..." claims
Pat from "Cannabis
vs Dilantin. Safety Ratio. WoDs, etc.", Marihemp, July 2 2000.

1988: "Patient evaluations have indicated that approximately ninety-three
(93) percent of marijuana inhalation treatment episodes are reported to be
'effective' or 'highly effective' when compared to other antiemetics." 78%
of 56 patients had no improvement with standard antiemetics, claims Vinciguerra,
et al, "Inhalation Marijuana as an Antiemetic for Cancer Chemotherapy", New
York State Journal of Medicine, pgs 525-527, Oct 1988.

1983: Inhaled botanical cannabis is "far superior to the best available
conventional drug, Compazine, and clearly superior to synthetic THC pill."
claims the report of The Lynn Pierson Therapeutic Research Program, Behavioral
Health Sciences Div, Health and Environment Department, State of New Mexico.

1981: "74 percent of the cancer patients treated in the program have
reported that [inhaled] marijuana is more effective in relieveing their nausea
and vomiting than any other drug they have tried." claims California Research
Advisory Panel, Annual Report of the California Research Advisory Panel,
vol 12, submitted to the Governor and Legislature.

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ...
My neurologist prescribed the drugs Compazine and Antivert. They had little
affect on the nausea and no affect on the appetite, even after the dosage
was doubled. After a couple of weeks of feeling sick and not eating, I had
lost 15 pounds and no medication was helping. ... I decided to try smoking
Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke
were gone I began to relax and get an appetite. I could finally eat again.
Since that time, I have used cannabis to maintain a healthy body weight and
a decent standard of living. For years I left my prescription drugs setting
on the counter, as Cannabis was more effective." claims John E Precup from
"Patient
Testimonials"

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... There are occasions when he is
seen in the office or the emergency room and given shots of Demerol [meperidine]
and Phenergren [promethazine]. Even these shots do not give him full relief
of his headaches, but do, when things are severe, give him a few hours
of peace. The only drug that seems to give William any true felief from
pain is that from smoking marijuana. ... Having seen him in constant pain
without the availability of the Marinol or marijuana purchased from a street
dealer, I have no question that there is pain relief afforded to him by the
drug." claims Dr Michael E Mayle, DO, in a letter to Whom It May Concern,
1996.

2006: "The least physiologically toxic substances, those requiring
100 to 1,000 times the effective dose to cause death, include psilocybin
mushrooms and marijuana, when ingested. I've found no published cases in
the English language that document deaths from smoked marijuana, so the actual
lethal dose is a mystery." claims Robert
S Gable,
"The
Toxicity of Recreational Drugs", American Scientist, May-June
2006.

2005: "Cannabis-using Crohn's patients ... are
also able to reduce the amount of immunosuppressive medications that have
been a mainstay of conventional treatment. ... Steroids are noted to be reduced
and often eliminated. ... Steroids have a host of common side effects including
anxiety, depression, irritability, nausea, vomiting, abdominal pain; and,
with chronic use, bone thinning, glucose intolerance, peptic ulcers, and
the Cushingoid state." reports Jeff Hergenrather,
"Cannabis Alleviates
Symptoms of Chrohn's [sic] Disease", O'Shaughnessy's Journal of the
California Cannabis Research Medical Group, Autumn 2005.

"These [anti-inflammatory] drugs [Asacol, Azulfidine, Pentasa, Rowasa] provided
minimal to no relief from symptoms while causing kidney pain, burning urination,
significant loss of hair, further loss of appetite, and irritation to the
rectum.... Using marijuana provided great relief from the pain, cramping,
and nausea. It also resulted in fewer bowel movements each day, and increased
my appetite helping me keep a more stable body weight. I also noticed it
improved my mood so I wasn't feeling depressed all the time." claims anonymous
Arkansas man from
"Patient Story
- Ulcerative Colitis".

1988: "Patient evaluations have indicated that approximately ninety-three
(93) percent of marijuana inhalation treatment episodes are reported to be
'effective' or 'highly effective' when compared to other antiemetics." 78%
of 56 patients had no improvement with standard antiemetics, claims Vinciguerra,
et al, "Inhalation Marijuana as an Antiemetic for Cancer Chemotherapy", New
York State Journal of Medicine, pgs 525-527, Oct 1988.

1981: 95% of patients randomized to the antiemetic Torecan choose
to discontinue use of Torecan and switched to cannabis, claims "Michigan
Department of Public Health Marijuana Therapeutic Research Project, Trial
A 1980-81", Department of Social Oncology, Evaluation Unit, Michigan Cancer
Foundation, March 18, 1982.

1981: "74 percent of the cancer patients treated in the program have
reported that [inhaled] marijuana is more effective in relieveing their nausea
and vomiting than any other drug they have tried." claims California Research
Advisory Panel, Annual Report of the California Research Advisory Panel,
vol 12, submitted to the Governor and Legislature.

2013: "Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked.
In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by [the equivalent of]
40 percent during treatment.
... This is the first study, as far as we are aware, to demonstrate the impact of CBD on cigarette smoking. ...
These preliminary data, combined with the strong preclinical rationale for use of this compound,
suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration."
 "Cannabidiol reduces cigarette
consumption in tobacco smokers: Preliminary findings"
by Celia JA Morgan, Ravi K Das, Alyssa Joye, H Valerie Curran, Sunjeev K Kamboj,
Addictive Behaviors, vol 38 no 9, Sept 2013, pgs 2433-2436.

2008: "Cannabis smoking may be a risk factor for periodontal disease
that is independent of the use of tobacco. ... Tobacco smoking was strongly
associated with periodontal disease experience, but there was no interaction
between cannabis use and tobacco smoking in predicting the condition's
occurrence." claims W Murray Thomson, et al,
"Cannabis
Smoking and Periodontal Disease Among Young Adults", Journal of Amercian
Medical Association, Feb 6 2008

2006: "... Thomas Glynn, the ACS's director of cancer science and
trends, concedes that Swedish-style snuff (a.k.a. snus) 'may be less harmful
than other smokeless tobacco products and cigarettes,' ... First, there's
no 'may be'about it: Smokeless tobacco is indisputably much safer than
cigarettes. Second, while Swedish methods produce oral snuff with lower levels
of certain carcinogens than the old-style American process, all forms of
smokeless tobacco are much less hazardous than cigarettes. The difference
in risk between different kinds of oral snuff pales in comparison to the
huge difference in risk between oral snuff and cigarettes. ... Smokeless
tobacco is cheaper than other forms of nicotine replacement, it delivers
levels of nicotine closer to those smokers are used to, and in the form of
Swedish-style snus it poses negligible health risks. ..." claims Jacob Sullum
from
"Anti-Smokers
Inch Toward Pandora's Box of Snuff", Aug 11 2006.

2005: "A recent study in the Journal of Clinical Investigation
suggests that smoking pot can make the brain grow. Though most drugs
inhibit the growth of new brain cells, injections of a synthetic cannibinoid
have had the opposite effect in mice in a study performed at the University
of Saskatchewan. ... Many drugs  heroin,
cocaine, and the more common
alcohol and nicotine  inhibit the growth of
these new cells. It was thought that marijuana did the same thing, but this
new research suggests otherwise. ... The researchers found that rats treated
with HU-210 [a potent synthetic cannabinoid] on a regular basis showed
neurogenesis  the growth of new brain cells in the hippocampus. " reports
Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2005: "Marijuana smoking -'even heavy longterm use'- does not cause
cancer of the lung, upper airwaves, or esophagus,
Donald Tashkin reported at this
year's meeting of the International Cannabinoid Research Society. ... The
data on tobacco use, as expected, revealed 'a very potent effect and a clear
dose-response relationship -a 21-fold greater risk of developing lung cancer
if you smoke more than two packs a day.' Similarly high odds obtained for
oral/pharyngeal cancer, laryngeal cancer and esophageal cancer." reports
Fred Gardner from
"Study:
Smoking Marijuana Does Not Cause Lung Cancer", CounterPunch, July
2-4 2005.

2004: "A life of [tobacco] cigarette smoking will be, on average,
10 years shorter than life without it. ... almost half of all persistent
[tobacoo] cigarette smokers were killed by their habit, and a quarter died
before age 70. ... someone who stops [tobacco] smoking by age 30 has the
same average life expectancy as a nonsmoker, and someone who stops at
age 50 will lose four, rather than 10, years of life." claims Richard Doll
in British Medical
Journal, June 22 2004, as reported by Marc Kaufman, Washington
Post.

2003: "Researchers ... further noted that the total mortality risks
associated with marijuana use were lower than those for tobacco-cigarette
smoking for both men and women. from
"Marijuana
Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Jouurnal
of the California Cannabis Research Medical Group, Summer 2003.

2002: "Smoking pure marijuana is at least as harmful to lungs as smoking
tobacco, a report from the British Lung Foundation concludes. And in some
key ways, it may be more dangerous. For example, the BLF's review of previous
research highlights that just three marijuana joints a day causes the same
damage to the lung's airways as 20 cigarettes, mainly because of the way
joints are smoked. Individually, cannabis and tobacco produce the same
constituents and quantities of chemicals known to be toxic to respiratory
tissue, other than nicotine, the report says. But when cannabis and tobacco
are smoked together, the health effects are worse. ... Other points in the
report include: Tar from cannabis cigarettes contains up to 50 per cent higher
concentrations of carcinogens benzathracenes and benzpyrenes than tobacco
smoke. ... Lyndon Pugh, editor of pro-cannabis magazine CC Newz, is not impressed
by the report: 'These allegations have been made before countless times.
Lot of things are dangerous, like driving.' " claims Emma Young,
"Cannabis
smoking 'more harmful' than tobacco", New Scientist news service,
Nov 11 2002.

1997: "In summary, this study showed little, if any, effect of marijuana
use on nonAIDS mortality in men and on total mortality in women. ... The
risk of mortality associated with marijuana use was lower than that associated
with tobacco cigarette smoking." claims Stephen Sidney MD, Jerome E
Bech PhD, Irene S Tekawa MA, Charles P Quesenberry Jr PhD, and Gary
D Friedman MD from
"Marijuana
Use and Mortality", American Journal of Public Health, April,
1997.

2006: "Tysabri has been linked to a potentially fatal brain infection
called progressive multifocal leukoencephalopathy, or PML. The drug's
manufacturers voluntarily pulled it from the market last year, following
the deaths of two patients. The drug had been sold for just four months.
Dozens of multiple sclerosis patients told a Food and Drug Administration
advisory committee Tuesday that they should be allowed to choose whether
to take Tysabri. ... In statements frequently punctuated by sobbing pleas,
patients told the Peripheral and Central Nervous System Drugs advisory committee
that MS posed an even greater risk than did PML. ... Biogen Idec and Elan
withdrew Tysabri from the market in February 2005 after two patients in clinical
trials involving 7,000 people died of PML." reports Associated Press "FDA
panel mulls rare reversal on MS drug", Mar 8 2006

Crohn's Disease

2005: "For all signs and symptoms evaluated in the study, the patients
described marked improvements with the use of cannabis. Beneficial effects
were reported for appetite, pain, nausea, vomiting, fatigue, activity, and
depression. Patients also reported that cannabis use resulted in weight gain,
fewer stools per day and fewer flare-ups of less severity. ... Cannabis-using
Crohn's patients not only report significant relief of their symptoms, they
are also able to reduce the amount of immunosuppressive medications that
have been a mainstay of conventional treatment. Imuran, methotrexate, 6 MP,
and Remicade (an anti-TNF drug) are greatly reduced. Asacol and Pentasa brands
of Mesalamine, an anti-inflammatory medication
with immuno-modulating properties is also reduced in many cases.
Steroids are noted to be reduced and often eliminated.
The immunosuppressives cause the same side effects that the disease causes:
nausea, vomiting, abdominal pain, and diarrhea.
Mesalamine frequently was reported to cause rash,
itching, and photosensitivity. Steroids have a host
of common side effects including anxiety, depression, irritability, nausea,
vomiting, abdominal pain; and, with chronic use, bone thinning, glucose
intolerance, peptic ulcers, and the Cushingoid state. ... Some of the patients'
responses include these telling remarks: 'A terrific reliever of Crohn's
symptoms.', 'A more easily controlled medication than offered by pills.',
'Alcohol has been a big problem for me that I don't have with cannabis.',
'Only positive effects, no negative effects.', 'Best appetite stimulant,
very good calming effect.', 'Cannabis provides relief without knocking me
out or other bad side effects that I had with steroids.', 'I've committed
myself to this form of therapy, and my quality of life has improved by leaps
and bounds.', 'I've struggled for years with opiate addiction from chronic
pancreatitis cannabis lets me control my pain without being a slave
to opiates.', 'Marinol bothered my stomach I don't get sick, constipated,
or vomit with cannabis.' " reports Jeff Hergenrather,
"Cannabis Alleviates
Symptoms of Chrohn's [sic] Disease", O'Shaughnessy's Journal of the
California Cannabis Research Medical Group, Autumn 2005.

2005: "Cannabis-based drugs could offer treatment hope to sufferers
of inflammatory bowel disease, UK researchers report. Cannabis smokers with
inflammatory bowel disease (IBD) have often claimed that smoking a joint
seems to lessen their symptoms. So a group of researchers from Bath University
and Bristol University, both in the UK, decided to explore the clinical basis
for the claims. 'There is quite a lot of anecdotal evidence that using cannabis
seems to reduce the pain and frequency of Crohns disease and ulcerative
colitis ...' says Karen Wright, a pharmacologist at Bath University.
'Historically, it was smoked in India and China centuries ago for its
gastrointestinal properties.' ... To their surprise, the team discovered
CB1 cannabinoid receptors  which are known to be present in the brain
 in the endothelial cells which line the gut. 'I think they must be
involved in repairing the lining of the gut when it is damaged,' Wright says.
She deliberately damaged the cells to cause inflammation of the gut lining
and then added synthetically produced cannabinoids. 'The gut started to heal:
the broken cells were repaired and brought back closer together to mend the
tears,' ... Previous studies have shown that CB1 receptors located on the
nerve cells in the gut respond to cannabinoids by slowing gut motility, therefore
reducing the painful muscle contractions associated with diarrhoea. But Wright
and her team also discovered another cannabinoid receptor, CB2, in the guts
of IBD sufferers, which was not present in healthy guts. These receptors,
which also respond to chemicals in cannabis, appear to be associated with
apoptosis  programmed cell death  and may have a role in suppressing
the overactive immune system and reducing inflammation by moping up excess
cells, she suggests." reports Gaia Vince from
"Cannabis may
soothe inflamed bowels", New Scientist, Aug 1 2005.

2005: "I've managed a Crohn's affliction very well for 20 years, the
last 12 of them prescription free except for one month when upon getting
a colonoscopy and being willing to try something else, I agreed to try Pentasa
[Mesalamine]. I pooped my brains out almost immediately
and for the next 5 days in spite of taking the drug for only two, on the
maximum dose the doctor felt I needed. I had to work up to that dose slowly
after two weeks off of it, and it seemed to work, but then he wanted me to
take monthly blood tests! Needless to say, I'll never be back to that
doctor.
My secret weapon has always been marijuana against the
spasming and pains of Crohn's, but I've also learned a few other things that
are necessary to keep me healthy, that are more important. By itself, it
doesn't stop the flare-ups (and from my experience nothing does that doesn't
potentially carry bigger problems in the long run.) What it does do is ease
the pain, and calm the system - which stops most all further pain. But the
secret to successfully living with Crohn's for me has been balanced diet,
balanced vitamin supplement, and stress management including regular marijuana
smoking through a water pipe."
claims James Moore, Crohn's patient.

2004: "Cannabis extracts may be well suited to treatment of inflammatory
diseases due to their multiple mechanisms of action. THC seemingly alleviates
pain, spasm and diarrhoea, while the CBD component presents the likelyhood
of immunomodulatory benefits. One recently demonstrated CBD effect is its
ability to inhibit TFN-a (tissue necrosis factor-alpha), a proven mechanism
of other agents employed to treat inflammatory bowel disease." reports
"Which
Conditions Are Treatable With Cannabis?", O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Spring 2004, citing
"The nonpsychoactive cannabis constiuent cannabidiol is an oral anti-artritic
therapeutic in murine collagen-induced arthritis." by AM Mafait, R Gallily,
PF Sumariwalla, AS Malik, E Andreakos, R Mechoulam, et al, Proceedings
of National Academy of Sciences USA 2000;97(17), pgs 9561-9566.

Depression

2005: "We show that 1 month after chronic HU210 [a potent synthetic
cannabinoid] treatment, rats display increased newborn neurons in the hippocampal
dentate gyrus and significantly reduced measures of anxiety- and depression-like
behavior. Thus, cannabinoids appear to be the only illicit drug whose capacity
to produce increased hippocampal newborn neurons is positively correlated
with its anxiolytic- and antidepressant-like effects. ... To determine the
relationship between hippocampal neurogenesis and anxiolytic- and
antidepressant-like effects produced by chronic HU210, we examined the effects
of a selective destruction of the hippocampal neural stem cells on the behavioral
effects of chronic HU210. During the course of receiving chronic HU210
injections, 1 group of Long-Evans rats received two 5-Gy doses of x-rays
confined to a limited brain region including the hippocampus ... Because
two 5-Gy doses of x-rays were not found to alter the morphology and function
of mature neurons in the hippocampus, hypothalamus, and amygdala, our results
together suggest that chronic HU210 treatment reduced anxiety and depression,
likely via promoting hippocampal neurogenesis. It has been shown that acute,
high doses of CB1 agonists or cannabinoids produced anxiety-like effects
in ratsor depression-like effects in mice. We observed here that chronic
administration of high, but not low, doses of HU210 exerts anxiolytic- and
antidepressant-like effects. To make things more complicated, acute, low
doses of cannabinoids have been found to induce anxiolytic-like effects in
rodents. These complicated effects of high and low doses of acute and chronic
exposure to cannabinoids may explain the seemingly conflicting results observed
in clinical studies regarding the effects of cannabinoid on anxiety and
depression. In summary, since adult hippocampal neurogenesis is suppressed
following chronic administration of opiates,
alcohol, nicotine, and
cocaine, the present study suggests that cannabinoids
are the only illicit drug that can promote adult hippocampal neurogenesis
following chronic administration. Increased hippocampal neurogenesis appears
to underlie the mechanism of anxiolytic- and antidepressant-like effects
produced by a high dose of chronic HU210 treatment. The opposing effects
of high doses of acute and chronic cannabinoids, together with the
anxiolytic-like effects caused by a low dose of cannabinoids, may finally
explain discrepancies in the clinical study literature regarding the effects
of cannabinoid on anxiety and depression." claims Wen Jiang, Yun Zhang, Lan
Xiao, Jamie Van Cleemput, Shao-Ping Ji, Guang Bai, Xia Zhang,
"Cannabinoids
promote embryonic and adult hippocampus neurogenesis and produce anxiolytic-
and antidepressant-like effects",
Journal of Clinical Investigation,
Nov 1 2005. PDF

2005: "The researchers found that rats treated with HU-210 [a potent
synthetic cannabinoid] on a regular basis showed neurogenesis  the
growth of new brain cells in the hippocampus. A current hypothesis suggests
depression may be triggered when the hippocampus grows insufficient numbers
of new brain cells. If true, HU-210 could offer a treatment for such mood
disorders by stimulating this growth. Whether this is true for all cannabinoids
remains unclear, as HU-210 is only one of many and the HU-210 in the study
is highly purified." reports Juanita King from
"science:
Study shows marijuana increases brain cell growth",
The Peak, Oct 31 2005.
Study Text,
PDF

2002: "The link between regular cannabis use and later depression
and schizophrenia has been significantly strengthened by three new studies.
... One of the key conclusions of the research is that people who start smoking
cannabis as adolescents are at the greatest risk of later developing mental
health problems. Another team calculates that eliminating cannabis use in
the UK population could reduce cases of schizophrenia by 13 per cent. Until
now, say Rey and Tennant, there was 'a dearth of reliable evidence' to support
the idea that cannabis use could cause schizophrenia or depression. That
lack of good evidence 'has handicapped the development of rational public
health policies,' according to one of the research groups, led by George
Patton at the Murdoch Children's Research Institute in Melbourne, Australia.
The reason for the link is unclear. Social consequences of frequent cannabis
use include educational failure and unemployment, which could increase the
risk of depression. 'However, because the risk seems confined largely to
daily users, the question about a direct pharmacological effect remains,'
says Patton. ... The new analysis revealed a dose-dependant relationship
between the frequency of cannabis use and schizophrenia. This held true in
men with no psychotic symptoms before they started using cannabis, suggesting
they were not self-medicating. Finally, researchers led by Terrie Moffitt
at King's College London, UK, analysed comprehensive data on over 1000 people
born in Dunedin, New Zealand in 1972 and 1973. They found that people who
used cannabis by age 15 were four times as likely to have a diagnosis of
schizophreniform disorder (a milder version of schizophrenia) at age 26 than
non-users. But when the number of psychotic symptoms at age 11 was controlled
for, this increased risk dropped to become non-significant. This suggests
that people already at greater risk of later developing mental health problems
are also more likely to smoke cannabis. The total number of high quality
studies on cannabis use and mental health disorders remains small, stress
Rey and Tennant. And it is still not clear whether cannabis can cause these
conditions in people not predisposed by genetic factors, for example, to
develop them." claims Emma Young from
"Cannabis
link to mental illness strengthened", New Scientist news service,
Nov 21 2002.

2000: "I've heard that Dilantin is ~ the World's best anti-seizure
drug and that it can be a very effective, fast-acting anti-depressant. ...
the full suite of Cannabinoids from the Cannabis Plant perform together as
the World's most effective anti-seizure 'agent' or combination. Also, this
herbal extract blend of Cannabinoids is a very safe and effective anti-depressant
medicine ..." claims Pat from
"Cannabis vs
Dilantin. Safety Ratio. WoDs, etc.", Marihemp, July 2 2000.

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and
acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium to control the depression associated with
his constant turmoil. There are occasions when he is seen in the office or
the emergency room and given shots of Demerol [meperidine] and Phenergren
[promethazine]. Even these shots do not give him full relief of his headaches,
but do, when things are severe, give him a few hours of peace. The only
drug that seems to give William any true felief from pain is that from
smoking marijuana. ... Having seen him in constant pain without the availability
of the Marinol or marijuana purchased from a street dealer, I have no question
that there is pain relief afforded to him by the drug. It should be noted
that the Marinol only gives him partial and inadequate pain relief." claims
Dr Michael E Mayle, DO, in a letter to Whom It May Concern, 1996.

"I have now identified past episodes of double depression with chronic depression
starting in High School. I also have social phobias. ... I am presently taking
300mg/day of Effexor. The medication does help with the depression and with
the social phobia but it is not a cure all. The side effects for me are reduced
sexual drive and sexual dysfunction, greatly increased cravings for simple
carbohydrates and weird, intense and sometimes disturbing dreams. It is also
rather expensive at $140/month. Marijuana has a quick and in most cases
a very positive effect on my mood and social phobias. The main negative seems
to be related to its illegal status and the paranoia that causes. ... I have
noticed that very small dose will elevate my mood without me being spacey
or having problems with short term memory loss. ... After almost a year on
Effexor I got to the point that I could no longer handle the side effects.
When it came time to refill my prescription I decided not to and quit cold
turkey. I stayed stoned for the next two weeks and this really helped me
make the transition. As long as I stayed stoned I was okay but when I was
not the depression hit hard. If you have never been so depressed that suicide
makes sense it may be hard to understand what this is like. ... During this
period I did experiment with making marijuana cookies. I found that this
worked much better. The dose would kick in more slowly and would hold out
much longer. ... Marijuana did help me through some really rough times and
without it I likely would have committed suicide. It seems to me that pot
needs to be the first medication a person gets when they fall into a deep
depression especially if suicide is an issue. This would get the person out
of their depression quickly and would allow time to find the best long-term
meds. It is real sad for me to hear how teens that are suddenly taken off
pot after daily use all to often commit suicide. I believe that if someone
with undiagnosed depression is using pot to self medicate they are at a high
risk of suicide if they are taken off pot suddenly and the underlying depression
is not addressed." claims anonymous patient from
"Depression".

Diabetes

2013: "there are limited data regarding the relationship between cannabinoids
and metabolic processes. Epidemiologic studies have found lower prevalence rates of
obesity and diabetes mellitus in marijuana users compared with people who have never
used marijuana, suggesting a relationship between cannabinoids and peripheral metabolic processes."
claims Elizabeth A Penner, Hannah Buettner, Murray A Mittleman, from
"The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults".

2001: "I have been a diabetic for 25 of those years. During this time,
I have had amputations to both feet. I've also had a stroke and am on dialysis.
I have what is called neuropathy. This is a highly painful nerve disorder.
Sometimes the pain was so severe I would wish my hands were cut off. I was
taking 2800mg of Neuroten a day plus 4 to 6 Percocet. I also have severe
hypertension and take 100 mg of Zoloft. After two years I became so dependent
on the Percocet. I was taking sometimes more than 10 a day. Then I started
smoking marijuana. It helped me stop taking the narcotics. I have stopped
taking Percocet and take only 400mg of the Neuroten. My pain is gone. When
I get really hyper I take about three hits and stay calm for hours. This
dialysis really zaps your energy. But I take a few hits after treatment,
and have energy to function all day." claims anonymous patient from
"Patient
Story - Neuropathy", May 6 2001, updated July 19 2001.

"My sister died two years ago at the age of 71 from complications from diabetes.
... Prior to her death she was in extreme pain, and had great difficulty
in eating due to constant nausea in addition to the pain. The usually prescribed
pain killers dulled her thinking, and at the same time her tolerance to those
increased to the point that they did little good. ... Although she was terminal,
I cannot tell you how much the quality of her remaining days improved with
the use of marijuana." claims anonymous sibling from
"Relief
in Pain and Dying - Patient Story".

Dialysis

2001: "I have been a diabetic for 25 of those years. During this time,
I have had amputations to both feet. I've also had a stroke and am on dialysis.
I have what is called neuropathy. ... Then I started smoking marijuana. ...
This dialysis really zaps your energy. But I take a few hits after treatment,
and have energy to function all day." claims anonymous patient from
"Patient
Story - Neuropathy", May 6 2001, updated July 19 2001.

2004: "I'm fighting for the right to use cannabis to prevent
uncontrollable seizures where over 20 Rx meds and surgery have failed....
My mother has had epilepsy all her life. Most of her life she was able to
control her seizures with dilantin, Phenobarbital and most recently Tegretol.
About 5 years ago she started having auras and seizures that no prescription
medication was able to control. ... The reason I'm writing is because we
know that cannabis (marijuana) prevents her seizures. Not only do I know
this but there are thousands of other patients out there that know it. ...
The Ohio State Medical Society convened a committee that reported on the
medicinal properties of cannabis in 1860. W.P. Kincaid reported: I
have treated four cases of epilepsy with the hemp; two were permanently benefited
(at least to the present time); one temporarily, and one not at all.
Major pharmaceutical firms listed epilepsy as one of the conditions for which
cannabis was indicated either alone or as an ingredient in combination
preparations." claims "phatboy" 
"5000
year old drug prevents seizures.", Epilepsy Foundation eCommunities Forums,
Jan 8 2004.

2003: "Ingredients in marijuana and the cannabinoid receptor protein
produced naturally in the body to regulate the central nervous system and
other bodily functions play a critical role in controlling spontaneous seizures
in epilepsy, according to a new study by researchers at Virginia Commonwealth
University. The study, the first to look at marijuana and the brains
cannabinoid system in live animals with spontaneous, recurrent seizures,
suggests new avenues that researchers can explore in their search for
more-effective drugs to treat epileptic patients who dont respond to
todays anticonvulsant medications or surgery. ... '... individuals
both here and abroad report that marijuana has been therapeutic for them
in the treatment of a variety of ailments, including epilepsy,' says Dr.
Robert J. DeLorenzo, professor of neurology in the VCU School of Medicine.
'If we can understand how marijuana works to end seizures, we may be able
to develop novel drugs that might do a better job of treating epileptic
seizures.' DeLorenzo and his colleagues in the VCU Department of Neurology
and the Department of Pharmacology and Toxicology have been studying the
therapeutic effects of marijuana on epilepsy and other illnesses for more
than a decade. They were the first three years ago to show that cannabinoids
work at controlling seizures by activating a protein known as the CB1 receptor
that is found in the memory-related area of the brain, the nervous system
and other tissues and organs in the body. Research has shown that the CB1
receptor is responsible for the psychoactive effects of marijuana. It also
is responsible for controlling excitability and regulating relaxation. ...
The team injected chronically epileptic rats with different combinations
of six drugs: 1) an extract of marijuana, 2) two synthetic drugs that include
the key psychoactive ingredients in marijuana, 3) the common anticonvulsant
drugs Phenobarbital and phenytoin and 4) a drug to block the activation of
the CB1 receptor by cannabinoids in the brain. The marijuana extract and
synthetic marijuana drugs completely eliminated the rats seizures,
which averaged three over a 10-hour period. The Phenobarbital and phenytoin
failed to completely eliminate the seizures. Injection of the CB1 antagonist
significantly increased the both the duration and frequency of seizures,
in some cases to a level consistent with a severe, prolonged form of epilepsy
known as status epilepticus. 'This study indicates that cannabinoids may
offer unique advantages in treating seizures compared with currently prescribed
anticonvulsants,' DeLorenzo said. 'It shows not only the anticonvulsant activity
of exogenously applied cannabinoids but also suggests that the brains
cannabinoid system works to limit seizure duration by activating the CB1
receptor. Understanding the factors that contribute to seizure initiation
and termination has important implications for our ability to treat epilepsy
and for the potential development of novel anticonvulsant agents.' " claims
Robert J DeLorenzo from
"Marijuana
and its receptor protein in brain control epilepsy", VCU News, Sept 30
2003.

2000: "I've heard that Dilantin is ~ the World's best anti-seizure
drug and that it can be a very effective, fast-acting anti-depressant. Also,
as I recall, one animal study was done with Dilantin and it ~ significantly
extended the average lifespan of the animals. ... the full suite of Cannabinoids
from the Cannabis Plant perform together as the World's most effective
anti-seizure 'agent' or combination. Also, this herbal extract blend of
Cannabinoids is a very safe and effective anti-depressant medicine ..." claims
Pat from "Cannabis
vs Dilantin. Safety Ratio. WoDs, etc.", Marihemp, July 2 2000.

1990: "It wasn't until I used marijuana that my seizures went away.
For 10 years I was in good shape. Now, in the last 11 months since I've been
denied marijuana, I've had 85 petit mal seizures and two grand mal seizures."
claims Gordon Hanson, epilepsy patient,
after his release from jail.

Fibromyaliga

"Ten years ago, I was an addiction professional, working in a chemical dependency
program. I also worked in DWI programs. Five years ago, I was in an auto
accident that totaled my truck and me. ... my doctor diagnosed me with
fibromyaliga. I lived in chronic pain and soon discovered there was no relief
for it. I tried nonsteroidal anti-inflammatory drugs (NSAIDs) but they caused
me to have edema in my feet and legs. I tried muscle relaxants but they lost
their effectiveness at the prescribed dose and didn't work any better at
a higher dose. ... With trepidation I lit the pipe, drew deeply and inhaled.
I repeated this two or three times and slowly a deep peace settled over me.
My tight muscles began to relax, a big grin spread over my face and I felt
like the person I used to be, before the accident. I couldn't say I was totally
pain free but I wasn't consumed with it either. I felt slightly removed from
the pain in my body and slept better that night than I had in years. The
next morning l sat and dealt with the cognitive dissonance produced by the
idea of smoking reefer to control pain. I was an addiction professional,
had done my graduate training in that field and knew that marijuana had no
physically addictive qualities to it. ... I started researching medical use
of marijuana on the Internet. l quickly realized that use of marijuana didn't
equal abuse of marijuana. I read enough reports, studies and anecdotal reports
to believe l'd finally hit on the least harmful way for me to deal with chronic
pain." claims anonymous patient from
"My
Story".

Gastrointestinal Disorders

2005: "Cannabis-based drugs could offer treatment hope to sufferers
of inflammatory bowel disease, UK researchers report. Cannabis smokers with
inflammatory bowel disease (IBD) have often claimed that smoking a joint
seems to lessen their symptoms. So a group of researchers from Bath University
and Bristol University, both in the UK, decided to explore the clinical basis
for the claims. 'There is quite a lot of anecdotal evidence that using cannabis
seems to reduce the pain and frequency of Crohns disease and ulcerative
colitis ...' says Karen Wright, a pharmacologist at Bath University.
'Historically, it was smoked in India and China centuries ago for its
gastrointestinal properties.' ... To their surprise, the team discovered
CB1 cannabinoid receptors  which are known to be present in the brain
 in the endothelial cells which line the gut. 'I think they must be
involved in repairing the lining of the gut when it is damaged,' Wright says.
She deliberately damaged the cells to cause inflammation of the gut lining
and then added synthetically produced cannabinoids. 'The gut started to heal:
the broken cells were repaired and brought back closer together to mend the
tears,' ... Previous studies have shown that CB1 receptors located on the
nerve cells in the gut respond to cannabinoids by slowing gut motility, therefore
reducing the painful muscle contractions associated with diarrhoea. But Wright
and her team also discovered another cannabinoid receptor, CB2, in the guts
of IBD sufferers, which was not present in healthy guts. These receptors,
which also respond to chemicals in cannabis, appear to be associated with
apoptosis  programmed cell death  and may have a role in suppressing
the overactive immune system and reducing inflammation by moping up excess
cells, she suggests." reports Gaia Vince from
"Cannabis may
soothe inflamed bowels", New Scientist, Aug 1 2005.

2004: "Cannabis extracts may be well suited to treatment of inflammatory
diesases due to their multiple mechanisms of action. THC seemingly alleviates
pain, spasm and diarrhoea, while the CBD component presents the likelyhood
of immunomodulatory benefits. One recently demonstrated CBD effect is its
ability to inhibit TFN-a (tissue necrosis factor-alpha), a proven mechanism
of other agents employed to treat inflammatory bowel disease." reports
"Which
Conditions Are Treatable With Cannabis?", O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Spring 2004, citing
"The nonpsychoactive cannabis constiuent cannabidiol is an oral anti-artritic
therapeutic in murine collagen-induced arthritis." by AM Mafait, R Gallily,
PF Sumariwalla, AS Malik, E Andreakos, R Mechoulam, et al, Proceedings
of National Academy of Sciences USA 2000;97(17), pgs 9561-9566.

1971: "Marijuana smoking and intraocular pressure" by R Hepler and
I Frank, Journal of the American Medical Association, vol 217, pg
1932.

"... at least 10% of all cases fail to be completely controlled by available
prescriptive drugs. In some instances available glaucomic medications can
cause side-effects such as headaches, kidney stones, burning of the eyes,
blurred vision, cardiac arrhythmias, insomnia, and nervous anxiety. These
side-effects may become so severe that the patient must discontinue use.
Marijuana has shown promise as a possible glaucoma treatment in numerous
published studies. In controlled studies at UCLA, it was discovered that
patients smoking marijuana experienced, on average, a 30% drop in eye pressure.
The reduction was dose related and lasted 4 to 5 hours. Dr. Robert Hepler,
principal investigator in the UCLA study, concluded that cannabis may be
more useful than conventional medications and may reduce eye pressure in
a way that conventional medications do not, thus making marijuana a potential
additive to the glaucoma patient's regimen of available medication. Tolerance
to conventional medications is a common problem in glaucoma control. The
use of marijuana for additional IOP reduction could eliminate the need for
surgical intervention. Glaucoma surgery costs Americans an estimated $8.8
million per year. Scientists have been working to develop a marijuana eyedrop
for several years. Until recently, they concentrated on delta-9-THC, marijuana's
psychoactive ingredient. Some researchers, however, have begun to wonder
if other constituents in the cannabis plant might be more effective in reducing
IOP. This theory is bolstered by the few glaucoma patients who have continued,
legal access to marijuana. In these cases, synthetic THC is only effective
for a short period of time. Natural marijuana, however, consistently lowers
IOP. A number of pharmaceutical companies are investigating drugs that are
chemically similar to various constituents of cannabis for possible glaucomic
applications. A West Indies pharmaceutical company has developed a synthetic
marijuana eyedrop but this is unavailable in the U.S." claims Alliance for
Cannabis Therapeutics from
"Medical
Use of Marijuana by Patients with Glaucoma"

"... in 1974 ... a storm caused a no-fault head-on wreck ... I woke up from
a coma four days later ... I lost my left eye and the left side of my face
and jaw. ... I had injury-induced glaucoma in my right eye, according to
the opthamologist ... they put me on a steady diet of atropine and pilocarpene,
alternating doses. After stepping up the doses a year later, he declared
it was hopeless and said I'd be totally blind within a year. ... Pharmacopeias
and the U. S. Dispensary all refer to pharmaceutical grade cannabis. ...
I contacted Bob Randall, who was the first glaucoma patient to get legal
cannabis in the United States. He told me he smoked a joint of buds every
two hours (while awake) for over ten years, supplied by the government. He
was doing fine. ... I have over 25 years of drawing evidence of the positive
effects of steady use of cannabis. ... Cannabis improves the quality of my
illustration. It makes observation and concentration easier. ... One aspect
where cannabis definitely helps is on night vision. I grew up night hunting,
so I had plenty of experience before and after. I can definitely see better
at night now." claims anonymous patient from
"Patient
Story - Joe Smith - Glaucoma".

Habituation

2003: "The reportedly successful use of cannabis as an alternative
to alcohol, SSRI antidepressants, and stimulants (in
the treatment of ADHD) warrants serious, large-scale investigation. A necessary
first step is for the doctors who are monitoring patients using cannabis
for these purposes to agree on basic definitions, diagnostic criteria, etc.,
and to adopt uniform record-keeping methods. Hergenrathers observation
that half his cannabis-using patients have been able to stop taking
pharmaceutical drugs  and others have reduced their intake  suggests
a line of inquiry that belongs on a common interview form." claims
Fred Gardner from
"Which
Conditions are Californians Actually Treating With Cannabis?",
O'Shaughnessy's Jouurnal of the California Cannabis Research Medical
Group, Summer 2003.

1968: "There is no evidence that this activity [cannabis use] ...
is producing in otherwise normal people conditions of dependence or psychosis,
requiring medical treatment." claims British Advisory Committee on Drug
Dependence in The Wooten Report: Committee on Drug Dependence, Cannabis

1937: "... there is positively no evidence to indicate the abuse of
cannabis as a medicinal agent or to show that its medicinal use is leading
to the development of cannabis addiction. Cannabis at the present time is
slightly used for medicinal purposes, but it would seem worthwhile to maintain
its status as a medicinal agent for such purposes as it now has. There is
a possibility that a re-study of the drug by modern means may show other
advantages to be derived from its medicinal use." claims the AMA Committee
on Legislative Activities.

Hangover

Hashish

Headache

1998: "Cannabis, or marijuana, has been used for centuries for both
symptomatic and prophylactic treatment of migraine. It was highly esteemed
as a headache remedy by the most prominent physicians of the age between
1874 and 1942, remaining part of the Western pharmacopoeia for this indication
even into the mid twentieth century. Current ethnobotanical and anecdotal
references continue to refer to its efficacy for this malady, while biochemical
studies of THC and anandamide have provided a scientific basis for such
treatment." 
"Cannabis
for Migrane Treatment: The Once and Future Prescription?" by
Ethan B Russo, 1998.

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and
acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium to control the depression associated with
his constant turmoil. There are occasions when he is seen in the office or
the emergency room and given shots of Demerol [meperidine] and Phenergren
[promethazine]. Even these shots do not give him full relief of his headaches,
but do, when things are severe, give him a few hours of peace. The only
drug that seems to give William any true felief from pain is that from
smoking marijuana. ... Having seen him in constant pain without the availability
of the Marinol or marijuana purchased from a street dealer, I have no question
that there is pain relief afforded to him by the drug. It should be noted
that the Marinol only gives him partial and inadequate pain relief." claims
Dr Michael E Mayle, DO, in a letter to Whom It May Concern, 1996.

Heart

2005: "The active ingredient in cannabis protects arteries against
harmful changes that lead to strokes and heart attacks, new research suggests.
THC, or delta-9-tetrahydrocannabinol, is known to affect the brain and make
cannabis-users 'high'. The new research shows that it also has an influence
on blood vessels. A study of mice revealed that the compound blocks the process
of inflammation, which is largely responsible for the narrowing of arteries.
Inflammation combines with fatty deposits to produce obstructive 'plaques',
a condition known as atherosclerosis. These can block arteries to the heart,
causing angina and heart attacks, or to the brain, leading to strokes.
Atherosclerosis is the primary cause of heart disease and stroke in the Western
world, accounting for up to half the deaths from both conditions. The scientists,
led by François Mach, from Geneva University Hospital in Switzerland,
studied a strain of specially bred mice that are susceptible to narrowing
of the arteries. They were fed a high-cholesterol diet to make them develop
atherosclerotic plaques. Adding THC to their diet caused the growth of the
obstructions in their arteries to slow markedly after 11 months. When the
mice were given a chemical that blocked the action of THC, their arteries
continued to narrow at a fast rate." reports Nigel Hawkes, Times online,
Apr 7 2005.

2005: "The active ingredient of cannabis may protect against heart
disease and strokes ... If a similar effect can be demonstrated in people,
it would bring further ammunition to the camp of those who think that marijuana
(or rather its purified derivatives) should be treated seriously as a medicine.
Sadly for recreational users, though, the dose of THC required was very specific.
Too little or too much and the effect went away. Smoking spliffs is already
known to be bad for the heart. The protective effect Dr Steffens has demonstrated
is only limited compensation." claims Economist, Apr 7 2005.

2005: "Low doses of the main active ingredient in marijuana slowed
the progression of hardening of the arteries in mice, suggesting a hint for
developing a new therapy in people. ... The mouse work is presented
in Thursday's issue of the journal Nature by Dr. Francois Mach of
Geneva University Hospital in Geneva, Switzerland, and colleagues. ... Hardening
of the arteries sets the stage for heart attacks." reports Malcolm Ritter,
Associated Press, Apr 6 2005.

2000: "Dr. Murray Mittleman of the Harvard School of Public Health
and Boston's Beth Israel Deaconess Medical Center ... presented the data
at a conference in San Diego of the American Heart Association ... found
that the risk of a heart attack is five times higher than usual in the hour
after smoking a joint. To put this into perspective, many things can trigger
a heart attack, including just climbing out of bed in the morning. The
researchers said that for someone in good shape, marijuana is about twice
as risky as exercising or having sex. The researchers questioned 3,882 heart
attack victims - men and women - at 62 locations across the country about
their habits and found that 124 were marijuana users. While pot was uncommon
among the elderly heart patients, 13 percent of those under age 50 said they
smoke it. Among those questioned, 37 had their heart attacks within a day
of using marijuana, including nine within an hour afterward. The researchers
calculated that someone's risk of a heart attack is five times higher during
the hour after using marijuana. After an hour, the risk falls to twice normal.
It soon returns to the usual level." reports Daniel Q. Haney, Associated
Press Medical Editor, in "Study Marijuana Raies Heart Risks", March 3,
2000.
Rebuttal: "Mittleman['s] ... nurse/receptionist [was] ... asked about the
percentage of tobacco smoking in this relatively small
group of pot smokers [37] that had heart attacks, and in the overall group
of 3,882 heart attack patients. She told [Masel] that most were tobacco smokers
too, but she did not have the percentages ..." claims
Ben Masel.

1982: "[there is no evidence that smoking marijuana] exerts a permanently
deleterious effect on the normal cardiovascular system." claims Institute
of Medicine.

"The 'endogenous' cannabinoid anandamide was shown to lower blood pressure
and heart rate through the CB1 receptor. The CB1 antagonist SR141716 was
shown to block the blood-pressure-lowering effects of anandamide. The researchers
guessed that the CB1 receptors were lowering blood pressure by vasodilation
through the sympathetic nervous system." claims Los Angeles Cannabis Resource
Center from
"Cannabinoids in
the Brain".

"[Tashkin] noted that THC, the substance that produces a marijuana high,
speeds up the heart rate by 50 percent. At the same time, the amount of oxygen
available to the heart is reduced because of the carbon monoxide in the
marijuana. He said this combination of increased oxygen demand and reduced
oxygen supply could trigger a heart attack,"  Associated Press review
of Dr Donald P Tashkin's research
published in New England Journal of Medicine.

Herpes

1991: "According to research by Dr. Gerald Lancz, Department of Medical
Microbiology and Immunology at the University of South Florida, there is
scientific support for the hemp herpes cure mentioned in the May '91 Letters."
reports Richard Doblin,
"Hemp Herpes Cure", High Times magazine, Aug 1991, pg 16.

1991: "A while back I wrote you concerning a treatment that I developed
for herpes: Mix one part Skunk bud to two parts rubbing alcohol until mixture
turns green; apply mixture every three to four hours onto affected area,
I have tried this on a couple of people with cold sores, as well as on people
with genital herpes. The treatment seems to kill the virus as it comes
to the surface, preventing it from multiplying and creating the characteristic
blister." claims Anonymous Experimenter, "Hemp Herpes Cure?", High Times magazine, May 1991.

Immune System

1989: "One study of marijuana use suggests that daily use for 9 weeks
restored initially low numbers of T lymphocytes to normal." claims Multicenter
AIDS Cohort Study in its report "No evidence for a Role of Alcohol or Other
Psychoactive Drugs in Accelerating Immunodeficiency in HIV-1 Positive
Individuals", Journal of the American Medical Association, June 16,
1989.

1992: "Despite the fairly large literature that developed during the
past 15 years or so, the effect of cannabinoids on the immune system is still
unsettled. The evidence has been contradictory and is more supportive of
some degree of immunosuppression only when one considers in vitro studies.
These have been seriously flawed by the very high concentrations of drug
used to produce immunosuppression and by the lack of comparisons with other
membrane-active drugs. The closer that experimental studies have been to
actual clinical situations, the less compelling has been the evidence. ...
The relationship between the use of social drugs and the development of clinical
manifestations of AIDS has been of some interest, however. Persons infected
with the virus but not diagnosed as AIDS have been told to avoid the use
of marijuana and/or alcohol. This advice may be reasonable
as a general health measure, but direct evidence that heeding this warning
will prevent the ultimate damage to the immune system is totally lacking."
claims Leo E Hollister from
"Marijuana
and Immunity", Journal of Psychoactive Drugs, Apr-June 1992, vol
24, pgs 159-163.

1989: "No evidence for a Role of Alcohol or Other Psychoactive Drugs
in Accelerating Immunodeficiency in HIV-1 Positive Individuals", Multicenter
AIDS Cohort Study, Journal of the American Medical Association, June
16, 1989.

1987: "Whatever temporary changes marijuana may produce in the immune
system, they have not been found to increase the danger of infectious disease
or cancer. If there were significant damage, we might expect to find a higher
rate of these diseases among young people beginning in the 1960s, when marijuana
first became popular. There is no evidence of that." claims
Lester A Grinspoon, MD, "Marijuana",
The Harvard Medical School Mental Health Letter, Nov 1987, pg 3.

"Studies on certain species of rats using high doses of THC showed observable
suppression of the immune system and the actions of 'tumoricidal' cells.
This evidence suggests that the wonderful auto-immune-disease-curative powers
of THC measured in 1989 ... has a negative side to it - perhaps THC allows
cancer and opportunistic infections to spread more easily? A report by the
National Toxicology Program failed to support this notion. As described in
AIDS Treatment News, the research project tested rats for two years
with a steady dose of either THC or placebo. The THC dose was extremely high.
The rats on THC lived longer and developed fewer tumors than those on the
placebo. This report was not released on schedule and people have suggested
it was deliberately suppressed because the results were too shocking." claims
Los Angeles Canmnabis Resource Center form "Cannabinoids in the Immune System".

Inflammatory Bowel Disease (IBD)

2005: "Cannabis-based drugs could offer treatment hope to sufferers
of inflammatory bowel disease, UK researchers report. Cannabis smokers with
inflammatory bowel disease (IBD) have often claimed that smoking a joint
seems to lessen their symptoms. So a group of researchers from Bath University
and Bristol University, both in the UK, decided to explore the clinical basis
for the claims. 'There is quite a lot of anecdotal evidence that using cannabis
seems to reduce the pain and frequency of Crohns disease and ulcerative
colitis ...' says Karen Wright, a pharmacologist at Bath University.
'Historically, it was smoked in India and China centuries ago for its
gastrointestinal properties.' ... To their surprise, the team discovered
CB1 cannabinoid receptors  which are known to be present in the brain
 in the endothelial cells which line the gut. 'I think they must be
involved in repairing the lining of the gut when it is damaged,' Wright says.
She deliberately damaged the cells to cause inflammation of the gut lining
and then added synthetically produced cannabinoids. 'The gut started to heal:
the broken cells were repaired and brought back closer together to mend the
tears,' ... Previous studies have shown that CB1 receptors located on the
nerve cells in the gut respond to cannabinoids by slowing gut motility, therefore
reducing the painful muscle contractions associated with diarrhoea. But Wright
and her team also discovered another cannabinoid receptor, CB2, in the guts
of IBD sufferers, which was not present in healthy guts. These receptors,
which also respond to chemicals in cannabis, appear to be associated with
apoptosis  programmed cell death  and may have a role in suppressing
the overactive immune system and reducing inflammation by moping up excess
cells, she suggests." reports Gaia Vince from
"Cannabis may
soothe inflamed bowels", New Scientist, Aug 1 2005.

2004: "Cannabis extracts may be well suited to treatment of inflammatory
diseases due to their multiple mechanisms of action. THC seemingly alleviates
pain, spasm and diarrhoea, while the CBD component presents the likelyhood
of immunomodulatory benefits. One recently demonstrated CBD effect is its
ability to inhibit TFN-a (tissue necrosis factor-alpha), a proven mechanism
of other agents employed to treat inflammatory bowel disease." reports
"Which
Conditions Are Treatable With Cannabis?", O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Spring 2004, citing
"The nonpsychoactive cannabis constiuent cannabidiol is an oral anti-artritic
therapeutic in murine collagen-induced arthritis." by AM Mafait, R Gallily,
PF Sumariwalla, AS Malik, E Andreakos, R Mechoulam, et al, Proceedings
of National Academy of Sciences USA 2000;97(17), pgs 9561-9566.

Inhalation

1996: 80% of AIDS patients who had used inhaled cannabis preferred
it to prescription drugs including synthetic THC, claims B Wesner, "The Medical
Marijuana Issue Among PWAs: Reports of Therapeutic Use and Attitudes Toward
Legal Reform", Drug Research Unit, Social Science Research Institute, University
of Hawaii at Manoa.

1993: "This water pipe study is a classic example of the harm reduction
approach to drug use. If water pipes really reduce the harm associated with
marijuana smoking, non-medical users can be educated about the benefits of
water pipes and encouraged to use them whenever possible. Since smoking is
one of the main harms associated with the use of marijuana (accidents are
another), this simple water pipe study may help lay the groundwork for
significantly reducing the harmfulness of marijuana smoke. If US drug policy
ever moves to a harm-reduction approach to marijuana, studies such as this
one will play an important role in helping users to identify and minimize
the health risks of marijuana." claims
Dale Gieringer,
"Marijuana
Water Pipe Study", Newsletter of the Multidisciplinary Association
for Psychedelic Studies, Vol 4, No 3, Winter 1993-94.

1988: "Marijuana cigarettes in many cases are superior to synthetic
THC capsules in reducing chemotherapy-induced nausea and vomiting. Marijuana
cigarettes have an important, clear advantage over synthetic THC capsules
in that natural marijuana is inhaled and generally takes effect more quickly
than the synthetic capsule." claims Drug Enforcement Administration's Chief
Administrative Law Judge Francis L
Young.

1988: "Patient evaluations have indicated that approximately ninety-three
(93) percent of marijuana inhalation treatment episodes are reported to be
'effective' or 'highly effective' when compared to other antiemetics." 78%
of 56 patients had no improvement with standard antiemetics, claims Vinciguerra,
et al, "Inhalation Marijuana as an Antiemetic for Cancer Chemotherapy", New
York State Journal of Medicine, pgs 525-527, Oct 1988.

1983: "We found both marijuana smoking and THC capsules to be effective
antiemetics. We found an approximate 23 percent higher success rate among
those patients smoking (90%) than among those administered THC capsules (67%).
... We found that the major reason for smoking failure was smoking intolerance;
while the major reason for THC capsule failure was nausea and vomiting so
severe that the patient could not retain the capsule." claims "Annual Report:
Evaluation of Marijuana and Tetrahydrocannabinol in the Treatment of Nausea
and/or Vomiting Associated with Cancer Therapy Unresponsive to Conventional
Anti-Emetic Therapy: Efficacy and Toxicity", Board of Pharmacy, State of
Tennessee, July 1983.

1983: "The primary reasons for failure of THC capsules were due to
either adverse reaction (6 out of 18) or failure to improve nausea and vomiting
(9 out of 18). The primary reason for failure of smoking marijuana were due
to smoking intolerance (6 out of 14) or failure to improve the nausea and
vomiting (3 out of 14)." claims Michael H Kutner, Evaluation of the Use
of Both Marijuana and THC in Cancer Patients for the Rel;ief of Nausea and
Vomiting Associated with Cancer Chemotherapy After Failure of Conventional
Anti-Emetic Therapy: Efficacy and Toxicity, Emory University, Atlanta,
GA, prepared for Composite State Board of Medical Examiners, Georgia Department
of Health, Jan 20, 1983.

1983: "[Inhaled] Marijuana has been shown to be effective for many
cancer chemotherapy patients, safe dosage levels have been established and
a dosage regimen which minimizes undesirable side effects has been devised
and tested." claims California Research Advisory Panel, Annual Report
of the California Research Advisory Panel, vol 14, submitted to the Governor
and Legislature.

1981: "74 percent of the cancer patients treated in the program have
reported that [inhaled] marijuana is more effective in relieveing their nausea
and vomiting than any other drug they have tried." claims California Research
Advisory Panel, Annual Report of the California Research Advisory Panel,
vol 12, submitted to the Governor and Legislature.

Insomnia

"For THC, the cannabinoid synthesized by cannabis sativa and indica, and
andandamide, the cannabinoid synthesized in the central nervous systems of
most animals on Earth, the receptor antagonist is called SR141716. SR141716
is like 'anti-marijuana'  it enhances the same memory functions that
the natural brain cannabinoid anandamide and THC inhibit through the cannabinoid
receptor. SR141716 improves short term memory in rodents by blocking the
CB1 cannabinoid receptor from binding to andandamide, not just THC. But
anandamide is made by the brain naturally. Why would the brain be making
a chemical  andandamide  that seems to inhibit short-term memory?
This question is partly answered by the effect of SR141716 on the sleep cycles
of rats. SR141716 administered to rats interrupts their sleep cycles, causing
a deficit in both short-wave and REM sleep. This research indicates that
cannabinoids are important in the brain's regulation of the sleeping process.
The cost of improving short-term memory by blocking cannabinoids from the
brain is deficient and delayed slow-wave and REM sleep. In studying marijuana,
we have learned something important about the brain. Inhibition of short-term
memory-related processes occurring ion the hippocampus might be necessary
for a healthy sleep cycle." claims Los Angeles Cannabis Resource Center
from "Cannabinoids
in the brain".

2004: "Another important question about the effects of drug policies
concerns the use of other illicit drugs. The 'separation of markets,' in
which lawfully regulated cannabis distribution reduces the likelyhood that
people seeking cannabis will be drawn into deviant subcultures where 'hard
drugs' also are sold is one public health objective of Dutch decriminalization.
... We compared representative samples of experienced cannabis users in similar
cities with opposing cannabis policies  Amsterdam, the Netherlands
(decriminalization), and San Francisco, Calif (criminalization). We compared
age at onset, regular and maximum use, frequency and quantity of use over
time, intensity and duration of intoxication, career use patterns, and other
drug use. Results: With the exception of higher drug use in San Francisco,
we found strong similarities across both cities. We found no evidence to
support claims that criminalization reduces use or that decriminalization
increases use. Conclusions: Drug policies may have less impact on cannabis
use than is currently thought." claims Craig Reinarman, Peter DA. Cohen,
Hendrien L Kaal from
"The
Limited Relevance of Drug Policy: Cannabis in Amsterdam and in San
Francisco", American Journal of Public Health, vol 94, no 5, May
2004, pgs 836-842. Also at
regulatemarijuana.org/pdf/ajph_050104.pdf

2003: "Other countries with high levels of cannabis use included very
prohibitionist France, (17 per cent), Spain (17.3 per cent) and Ireland (17.7
per cent), while in the Netherlands, where is has been available in coffee
shops for over 25 years, it was only 11.8 per cent. It is clear that the
laws have no effect on the rate of cannabis use, nor does the level of
enforcement." claims Richard Cowan
from his analysis of
"Marijuana
Arrests For 2002 Near Record High Despite Feds' War On Terror, FBI Report
Reveals", MarijuanaNews.com, Oct 28 2003.

1995: "... the 1976 changes in the Netherlands seem to have been followed
by a fall in use of cannabis: from 13% of those aged 17-18 in 1976 to 6%
in 1985. Monthly prevalence of cannabis use among Dutch high school students
is around 5.4% compared with 29% in the United States. Forbidden fruit may,
indeed, be the sweetest." claims British Medical Journal, Dec 1995.

1981: "Decriminalization has had virtually no effect either on the
marijuana use or on related attitudes and beliefs about marijuana use among
American young people." claims Lloyd Johnston, Patrick O'Malley, Jerald Bachman,
"Marijuana Decriminalization: The Impact on Youth, 1975-1980", Monitoring
the Future Occasional Paper 13, Institute for Social Research, Ann Arbor,
MI, 1981.

Longevity

Includes life expectancy, mortality

2004: "A life of [tobacco] cigarette smoking
will be, on average, 10 years shorter than life without it. ... almost half
of all persistent [tobacoo] cigarette smokers were killed by their habit,
and a quarter died before age 70. ... someone who stops [tobacco] smoking
by age 30 has the same average life expectancy as a nonsmoker, and someone
who stops at age 50 will lose four, rather than 10, years of life." claims
Richard Doll in
British Medical
Journal, June 22 2004, as reported by Marc Kaufman, Washington
Post.

2003: "Although the inhalation of chemical toxins in cannabis smoke
has been linked to bronchitis and other respiratory problems, it has not
been shown to cause lung cancer or a higher death rate. The most extensive
study to date on marijuana and mortality was conducted by investigators at
Kaiser Permanente and published in the April 1997 issue of the American
Journal of Public Health. It showed no substantial link between regular
marijuana smoking and death, but suggested that marijuana prohibition may
itself pose a health hazard to the user. The Kaiser team, led by Stephen
Sidney, MD, looked at 10 years of mortality statistics for more than 65,000
men and women who received health check-ups at Kaisers Oakland and
San Francisco hospitals between 1979 and 1985. Patients were divided into
groups ranging from those who had never tried marijuana to those who use
it currently or regularly. Mortality statistics for all patients were followed
until 1991 and analyzed for any association between marijuana and death.
The studys statistical methodology controlled for the use of
tobacco and alcohol so that
deaths from marijuana smoking could be clearly defined. Researchers found
no increase in deaths among the more than 14,000 patients who reported they
were marijuana users as compared to those who had never used marijuana. They
further noted that the total mortality risks associated with marijuana use
were lower than those for tobacco-cigarette smoking for both men and women.
Women who used marijuana also had a lower risk of total mortality as compared
to those who consumed alcohol regularly. The study noted that marijuana smokers
with AIDS did have a significantly higher death rate than non-smokers, but
said that their mortality was virtually the same as it was for AIDS patients
who didnt smoke marijuana. Researchers stressed that the links they
found between marijuana use and death were associations and not an indication
that marijuana was a cause of death. from
"Marijuana
Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Jouurnal
of the California Cannabis Research Medical Group, Summer 2003.

2000: "Marijuana-like drugs eradicated some brain cancers in rats
and helped other animals live longer, possibly hinting at a new approach
for treating the disease ... The study dealt with gliomas, the most common
category of cancer arising in the brain. Gliomas are highly lethal in people
despite treatment with drugs, surgery and radiation. The rat study was published
in the March issue of the journal Nature Medicine. It was conducted
by scientists at the Complutense and Autonoma Universityersities in Madrid,
Spain. They injected glioma cells into the brains of rats to produce tumors.
Untreated rats died within 18 days. Other rats were treated with drug infusions
for seven days through a tube leading to the tumor. Fifteen rats got infusions
of THC, the main active component in marijuana. Tumors disappeared in three
animals, and nine other rats outlived the untreated ones, surviving up to
35 days. When researchers used a different but similar drug, five of 15 rats
became tumor-free and four others outlived untreated animals."  Associated
Press, "Dope Ingredient May Fight Cancer", Feb 28, 2000.

1997: "In summary, this study showed little, if any, effect of marijuana
use on nonAIDS mortality in men and on total mortality in women. The increased
risk of AIDS mortality in male marijuana users probably did not reflect a
causal relationship, but most likely represented uncontrolled confounding
by male homosexual behavior. The risk of mortality associated with marijuana
use was lower than that associated with tobacco cigarette
smoking." claims Stephen Sidney MD, Jerome E Bech PhD, Irene S
Tekawa MA, Charles P Quesenberry Jr PhD, and Gary D Friedman MD from
"Marijuana
Use and Mortality", American Journal of Public Health, April,
1997.

1973: "The price of overuse is paid later in lifecannabis reduces
life expectancy from about seventy-five years to seventy." claims Dr W D
M Paton in testimony before US Senate Committee on Internal Security.

2003: "Although the inhalation of chemical toxins in cannabis smoke
has been linked to bronchitis and other respiratory problems, it has not
been shown to cause lung cancer or a higher death rate." 
"Marijuana
Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Summer 2003.

2002: "Smoking pure marijuana is at least as harmful to lungs as smoking
tobacco, a report from the British Lung Foundation
concludes. And in some key ways, it may be more dangerous. For example, the
BLF's review of previous research highlights that just three marijuana joints
a day causes the same damage to the lung's airways as 20 cigarettes, mainly
because of the way joints are smoked. Individually, cannabis and tobacco
produce the same constituents and quantities of chemicals known to be toxic
to respiratory tissue, other than nicotine, the report says. But when cannabis
and tobacco are smoked together, the health effects are worse. ... Other
points in the report include: Tar from cannabis cigarettes contains up to
50 per cent higher concentrations of carcinogens benzathracenes and benzpyrenes
than tobacco smoke. ... Lyndon Pugh, editor of pro-cannabis magazine CC Newz,
is not impressed by the report: 'These allegations have been made before
countless times. Lot of things are dangerous, like driving.' " claims Emma
Young,
"Cannabis
smoking 'more harmful' than tobacco", New Scientist news service,
Nov 11 2002.

1999: "Recent reports of molecular and genetic alterations in marijuana
users suggested that marijuana smoke might also activate CYP1A1 gene. Dr.
Roth investigated this possibility using Hepa-1 cells and found that marijuana
tar, and more specifically D9-THC, regulates the induction and function of
CYP1A1 gene, an observation that is entirely novel. Transcriptional activation
of CYP1A1 by D9-THC may help to explain the relatively high frequency of
DNA mutations and mucosal abnormalities that occur in marijuana smokers.
The inhalation of marijuana smoke delivers both nanogram concentrations of
conventional PAHs and milligram quantities of D9-THC to the lung. Induction
of CYP1A1 produced by D9-THC could result in greater activation of smoke-related
procarcinogens and higher adduct-related injury. However, it is also possible
that inhaled D9-THC competes for the active site of CYP1A1, paradoxically
reducing the activation of procarcinogens." claims Dr
Michael D Roth from
"A Conference Summary
on Pulmonary Pathophysiologic and Immune Consequences of Smoked Substance
Abuse", National Institute on Drug Abuse.

1998: "I said, 'Do you know of any cases of marijuana-only smokers
who had lung cancer?' [Dr Donald
P Tashkin] said 'Yes, there is one.' Then he smiled, explaining,
'He was sixteen years old.' We both smiled, knowing a teenager could not
possibly have sufficient exposure to marijuana smoke to cause lung
cancerhis cancer was clearly due to some other cause." claims Martin
Martinez from
"Cannabis
and Lung Cancer".

1997: "We evaluated the function of alveolar macrophages (AMs) recovered
from the lungs of nonsmokers and habitual smokers of either tobacco, marijuana,
or crack cocaine. AMs recovered from marijuana smokers were deficient in
their ability to phagocytose Staphylococcus aureus (p < 0.01). AMs from
marijuana smokers and from cocaine users were also severely limited in their
ability to kill both bacteria and tumor cells (p < 0.01). ... AMs are
the predominant lung leukocyte and act as the lung's resident phagocytic
defense against both bacteria and fungi. They secrete a variety of cytokines
capable of regulating their own activity, as well as the activity of other
immune effector cells. In addition, AMs are exposed to the highest possible
concentrations of inhaled marijuana and cocaine, making them a likely target
for drug-related effects. Our findings clearly demonstrate that habitual
smoking of either substance significantly impairs the antibacterial and
tumoricidal activities of human AMs, as well as, in the case of marijuana,
their ability to produce inflammatory cytokines. ... our findings strongly
support epidemiologic reports and case studies linking the use of marijuana
and cocaine to opportunistic infections, HIV infection, and the progression
of AIDS. In addition, marijuana may play a multifactorial role in the
pathogenesis of respiratory tract cancers." claims Gayle Cocita Bladwin,
Donald P Tashkin, Dawn M Buckley,
Alice N Park, Steven M Dubinett, Michael
D Roth from
"Marijuana
and Cocaine Impair Alveolar Macrophage Function and Cytokine Production",
American Journal of Respiratory and Critical Care Medicine, Vol 156, No 5,
Nov 1997, pgs 1606-1613.

1994: "Some forms of lung irritation may be more pronounced with chronic
marijuana smoke, but no signs of cancer were seen seven months after the
last dose" claims Dr. William Slikker,
Jr, researcher for a 2-1/2 year study of cannabis consumpt ion by youth
for the National Center of Toxicological Research, Jefferson, AR.

1993: "Marijuana smokers in our study also reported a higher prevalence
of upper respiratory tract infections compared with nonsmokers. On the other
hand, the duration of marijuana smoking appeared to be inversely related
to the risk of outpatient visits for respiratory problems. This result was
contrary to our expectation and remains an issue for future research. In
our data, long-term marijuana smokers may be the 'survivors' of a selection
process in which persons who experienced respiratory symptoms were more likely
to quit smoking marijuana early in the process." claims Michael R Polen,
Stephen Sidney, Irene S Tekawa, Marianne Sadler, and Gary D Friedman from
Health Care Use by Frequent Marijuana Smokers Who Do Not Smoke Tobacco",
Western Journal of Medicine #158, June 1993, pgs 596-601.
pbs.org/wgbh/pages/frontline/shows/dope/body/healthcare.html,
hoboes.com/pub/Prohibition...,
web.acsalaska.net/~warmgun/sm405.html

1988: "As of October 1988, no case of lung cancer has ever been attributed
solely to marijuana use." claims Dr
Donald P Tashkin.

1985: "The result is that there is a four-fold greater burden of tar
on the lung from the smoke of a single marijuana joint compared to one
cigarette when each type is smoke [sic] the way it's
ordinarily smoked,' Tashkin said. Tashkin said he believes this poses a
significant cancer risk, although there is no direct evidence that pot smokers
actually suffer an unusually high incidence of lung cancer. ... Tashkin said
his studies have not found any evidence that pot smoking increases risk of
emphysema ..."  Associated Press review of Dr
Donald P Tashkin's research
published in New England Journal of Medicine.

Manic Depression

2001: "I have smoked weed off and on for 20 years, and now everyday.
I find that with it I take less Paxil, and I am able to function better.",
Manic-depression/obsessive compulsive disorder patient, Mar 11, 2001.

1997: "American Medical Association and most other professional medical
bodies do not consider marijuana a safe or effective medicine. Other medical
organizations which oppose the use of smoked marijuana in treatment include
the American Cancer Society, the American Academy of Ophthalmology, the National
Multiple Sclerosis Association [sic], the National Eye Institute, the National
Cancer Institute, the National Institute for Neurological Disorders and Stroke,
and the California Medical Association." claims "Marijuana: Myths and Truth",
US Office of National Drug Control Policy. (see
American Cancer Society,
American Medical Association,
California Medical Association,
Patients Out of Time's Rebuttal)

1997: "... American Glaucoma Society and the American Academy of
Ophthalmology have both rejected marijuana has [sic] a treatment for glaucoma.
Other major medical and health organizations have concluded that smoking
marijuana is not safe and effective medicine. These organizations include
the American Medical Association, the International Federation of Multiple
Sclerosis, the American Cancer Society, and the National Cancer Institute."
claims "Executive Summary: Anti-legalization Issues", US Drug Enforcement
Administration. (seeAmerican Cancer Society,
American Medical Association)

1996: "AIDS Action Council supports the elimination of federal
restrictions that bar doctors from prescribing marijuana for medical use
by individuals with HIV/AIDS. ... AIDS Action Council supports reopening
the U.S. Public Health Service's Investigational New Drug Compassionate Access
program to provide access to medical-use marijuana for greater numbers of
qualified patients."  "Resolution in Support of Access to Medical-Use
Marijuana," adopted by the Public Policy Committee of AIDS Action Council,
Nov 15 1996.

1998: "The Alaska Nurses Association supports the passage of Ballot
Measure #8 [which] ... allow[s] patients to use marijuana as a medicine if
they have a debilitating disease and an authorization from their doctor."
 ANA Resolution, Sept 1998.

1996: "The American Academy of Family Physicians [supports] the use
of marijuana ... under medical supervision and control for specific medical
indications."  1996-1997 AAFP Reference Manual - Selected Policies
on Health Issues.

1997: "[California Senate Bill] 535 focuses on medical marijuana research.
[The] American Cancer Society ... supports S.B. 535 because it is consistent
with our long-held position of supporting research of any agent or technique
for which there may be evidence of a therapeutic advantage." in a letter
to California State Senator John Vasconcellos, July 24 1997.

2008: "We felt the time had come to speak up about this. We'd
like to clear up the uncertainty and anxiety of patients and physicians
over this drug." states American College of Physicians Pres David Dale.

2008: American College of Physicians supports therapeutic cannabis
research, rescheduling of cannabis and removal of criminal penalties for
therapeutic cannabis use, approved by ACP's governing board of regents and
published Feb 14 2008 in a 13 page declaration.
naturalnews.com/023172.html

2009: AMA "urges that marijuana's status as a federal Schedule I
controlled substance be reviewed with the goal of facilitating the conduct
of clinical research and development of cannabinoid-based medicines, and
alternate delivery methods."

1997: AMA's House of Delegates votes to adopt a report that recognizes
the existence of scientific clinical data showing cannabis' medical value,
urges doctors and patients not be punished for discussing cannabis as a treatment
option, and urges the United States government to expedite medicinal cannabis
research.

1997: "The American Medical Association 'states in view of the need
for further research, a policy of discouragement be strongly advocated' toward
prescribing marijuana, the group said in a policy statement." claims David
Wahlberg, "Rise in teen marijuana use is focus of forums" by Wahlberg, Ann
Arbor News, Feb 17, 1997.

1995: "We are not asking readers for immediate agreement with our
affirmation that marijuana is medically useful, but we hope they will do
more to encourage open and legal exploration of its potential."  an
editorial, Journal of the American Medical Association, 1995.

1989: "One study of marijuana use suggests that daily use for 9 weeks
restored initially low numbers of T lymphocytes to normal." claims Multicenter
AIDS Cohort Study in its report "No evidence for a Role of Alcohol or Other
Psychoactive Drugs in Accelerating Immunodeficiency in HIV-1 Positive
Individuals", Journal of the American Medical Association, June 16,
1989.

1989: "Large doses may result in panicky states, fear of death, and
illusions. Rarely, true psychosis (loss of contact with reality) occurs,
producing paranoid delusions, confusion, and other symptoms. These symptoms
usually disappear within several days if triggered by the drug, which may
merely be acting on an underlying illness. A more permanent state of apathy
and loss of concernthe amotivational syndromehas been attributed
to prolonged, regular use. There is evidence that regular users of marijuana
can become physically dependent on its effects. Whether the drug causes brain
or other physical damage is much debated." claims American Medical Association
Home Medical Encyclopedia, published by Reader's Digest, 1989.

1961: Joint Committee of the American Bar Association and the AMA
on Narcotic Drugs publishes report Drug Addiction: Crime or Disease? Interim
and Final Reports .

1937: "... there is positively no evidence to indicate the abuse of
cannabis as a medicinal agent or to show that its medicinal use is leading
to the development of cannabis addiction. Cannabis at the present time is
slightly used for medicinal purposes, but it would seem worthwhile to maintain
its status as a medicinal agent for such purposes as it now has. There is
a possibility that a re-study of the drug by modern means may show other
advantages to be derived from its medicinal use." claims the AMA Committee
on Legislative Activities.

1993: "The American Medical Student Association strongly urges the
United States Government ... to meet the treatment needs of currently ill
Americans by restoring the Compassionate IND program for medical marijuana,
and ... reschedul[ing] marijuana to Schedule II of the Controlled Substances
Act, and ... end[ing] the medical prohibition against marijuana." AMSA
House of Delegates Resolution #12, March 1993.

2003: "The American Nurses Association will: ... Support the right
of patients to have safe access to therapeutic marijuana/cannabis under
appropriate prescriber supervision. Support the ability of health care providers
to discuss and/or recommend the medicinal use of marijuana without the threat
of intimidation or penalization. Support legislation to remove criminal penalties
including arrest and imprisonment for bona fide patients and prescribers
of therapeutic marijuana/cannabis."  ANA Resolution, June 2003.

1997: "Marijuana should be available for appropriate medicinal purposes,
when such use is in accordance with state law, and that physicians who recommend
and prescribe marijuana for medicinal purposes in states where such use is
legal, should not be censured, harassed, prosecuted or otherwise penalized
by the federal government." form "Medicinal Use of Marijuana" policy
statement, Dec 8 1997.

1995: APHA "... encourages research of the therapeutic properties
of various cannabinoids and combinations of cannabinoids, and ... urges the
Administration and Congress to move expeditiously to make cannabis available
as a legal medicine." Resolution #9513: "Access to Therapeutic
Marijuana/Cannabis", Nov 1995.

1997: "Approved medical uses for marijuana or [THC] for treatment
of glaucoma, illnesses associated with wasting such as AIDS, the emesis
associated with chemotherapy, or other uses should be carefully controlled.
The drug should be administered only under the supervision of a knowledgeable
physician."  "Statement on Marijuana," passed by ASAM Board of Directors,
Apr 16 1997

2004: "[Cannabis is] not going to cure the disease, but it will do
a lot to allieviate the pain and suffering of people with rheumatoid
arthritis. Cannabis is probably less harmful than other available painkillers.
This idea that people with rheumatoid arthritis will be sitting around smoking
joints and getting high is quite wrong; cannabis-based pain killers should
be taken very seriously."  ARC spokeswoman in
"Cannabis drug cuts
arthritis pain", BBC News, June 9 2004.

2001: "The Arthritis Research Campaign has welcomed the Home Secretary's
announcement that cannabis may be legalised for medicinal use. ... A spokeswoman
for the ARC said Mr Blunkett's announcement was good news for people who
risked imprisonment by using cannabis to relieve the pain of their arthritis.
Scientists at the ARC's Kennedy Institute in west London have shown that
cannabidiol - a natural constituent of cannabis that has no mind-altering
effects in its purified form - can ease the effects of collagen-induced arthritis
in mice; a disease which resembles human rheumatoid arthritis." 
"ARC
welcomes easing of cannabis laws", Aug 2001.

1999: "The AMA (NSW) encourage[s] the Carr Government
to introduce exemptions to current cannabis laws, which would allow the use
of the currently prohibited drug, in specific medical cases to alleviate
patient suffering and facilitate research."  "New Cannabis Exemption
Laws Needed for Medical Use", AMANSW press release, Sept 30 1999.

1999: "The AMA (NSW) encourage[s] the Carr Government
to introduce exemptions to current cannabis laws, which would allow the use
of the currently prohibited drug, in specific medical cases to alleviate
patient suffering and facilitate research."  "New Cannabis Exemption
Laws Needed for Medical Use", AMANSW press release, Sept 30 1999.

1999: BMA's Scottish Committee for Public Health recommends removing
penalties for recreational use of cannabis. "We want to encourage public
debate on this issue and examine the evidence, rather than [have] people
leaping to prejudice. ... I think more than half the population would support
legalization if you laid out the evidence." claims committee chairman Dr.
George Venters.

1997: "Present evidence indicates that [cannabinoids] are remarkably
safe drugs, with a side-effects profile superior to many drugs used for the
same indications. ... [The BMA] will urge the government to consider changing
the Misuse of Drugs Act to allow the prescription of cannabinoids to patients
with certain conditions causing distress that are not adequately controlled
by existing treatments."  BMA report "Therapeutic Uses of Cannabis",
Nov 1997.

1998: "The role of cannabinoids in modern therapeutics remains uncertain,
but the evidence shows that it would be irrational not to explore
it. The active components of a plant which has been prized as a medicine
for thousands of years should not be discarded lightly, and certainly not
through political expediency or as a casualty of the war on drugs." 
BMJ editorial, Apr 4 1998.

1998: "Due to the lack of scientific justification for Schedule I
classification of marijuana and the consequent virtual standstill in research
on its medical benefits or harm, CMA's Board of Trustees last week voted
to support efforts to reschedule marijuana. In addition, the Board supported
efforts to obtain federal approval for a safe, reliable source of marijuana
in California for research. Reacting to the hazardous and completely uncontrolled
distribution of marijuana for medical use through buyers clubs and street
sources, the Board also supported federal control over distribution for medical
use in California through closely regulated sources." reports CMA Info,
May 21 1998.

1997: "The CMA urge that carefully designed, controlled clinical trials
of the effectiveness of inhaled marijuana for medical indications be allowed
to proceed immediately. ... The CMA immediately initiate efforts at the fed
eral level to facilitate the availability of inhaled marijuana for use in
conducting clinical research to determine the medical efficacy of marijuana."
 "Medical Marijuana", CMA Resolution #107a-97, adopted April 1997.

1997: "CSAM supports controlled studies of the medical usefulness
of marijuana, including all routes of administration, and especially supports
studies on the therapeutic effects of the essential ingredients ... of cannabis
s ativa. ... CSAM urges the DEA to remove cannabis from Schedule I and move
it to an appropriate Schedule, below Schedule I as determined by what is
known about its therapeutic benefit."  "Position on Medical Use of
Marijuana in California", California Society of Addicition Medicine
News, Spring 1997.

2004: "The Canadian AIDS Society's Board of Directors believes that
people living with HIV/AIDS should have access to cannabis for therapeutic
purposes in the treatment of HIV/AIDS through a compassionate framework.
... [We] favor a controlled legalization system for cannabis in Canada, where
the production, distribution and consumption are regulated, designated cannabis
distribution centres are established and recognized, and appropriate prevention
messages and harm reduction strategies are developed." adopted by the CAS'
Board of Directors, May 20 2004.

1995: "The Colorado Nurses Association recognize[s] the therapeutic
use of cannabis [and] support efforts to end federal policies which prohibit
or unnecessarily restrict marijuana's legal availability for legitimate health
care uses. ... Marijuana must be placed in a less restrictive Schedule and
made available to patients who may benefit from its use."  CNA 1995
Convention Directory and Book of Reports, pg 28.

1996: "The Congress of Nursing Practice ... support education for
RN's regarding current evidence based therapeutic uses of cannabis, [and]
support investigation of therapeutic efficacy of cannabis in controlled trials."
 Motion passed May 31 1996.

1997: "There is no problem, basically, with marijuana as a medicine.
... Marijuana is no different than morphine, no different
than codeine, no different than Aspirin." claims Health Canada spokesman
Dann Michols, Ottawa Citizen, Dec 19 1997.

2004: "It is the position of the Illinois Nurses Association to: Support
the right of patients to have safe access to therapeutic cannabis under
appropriate prescriber supervision; ... [to] support legislation to remove
criminal penalties including arrest and imprisonment for bonafide patients
and prescribers of therapeutic cannabis; [and to] support federal and state
legislation to include cannabis classification as a Schedule III [non-prohibited]
drug."  INA Position Statement, Dec 2004.

1997: "Be it resolved that this organization urges Congress and the
President to enact legislation to reschedule marijuana to allow doctors to
prescribe smokable marijuana to patients in need; and, Be it further resolved
that this organization urges the US Public Health Service to allow limited
access to medicinal marijuana by promptly reopening the Investigational New
Drug compassionate access program to new applicants." resolution approved
by Lymphoma Foundation Pres Belita Cowan, Jan 20 1997.

2004: "Assembly Bill 5796A ... would allow certain patients ... to
use marijuana to treat a serious condition that is defined as a life-threatening
condition or a condition associated with or a complication of such a condition
or its treatment. ... The Medical Society believes that this legislation
would provide physicians, in consultation with their patient, another treatment
option for those patients who are facing a life-threatening condition." 
MSSNY e-news, May 7 2004.

1995: "The Mississippi Nurses Association support all reasonable efforts
to end federal policies which prohibit or unnecessarily restrict marijuana's
legal availability for legitimate medical uses; and be it Resolved that the
Mississippi Nurses Association provide education to the nurses of Mississippi
about the therapeutic use of marijuana and federal prohibition of its use;
and be it Resolved that the Virginia Nurses Association encourage other health
care provider organizations to supp ort medical access to marijuana." Resolution
for Marijuana Access for Therapeutic Use, adopted by the MNA House of Delegates,
Oct 27 1995.

2001: "The MS Society of Canada welcomes Health Canada¹s initiative
providing a more compassionate system of possession and production for
individuals who feel they may benefit from the use of marijuana for medical
purposes.", from MS Society Viewpoint, July 2001.

2003: "People with MS have claimed that [marijuana] has helped them
to relieve a number of the symptoms of MS including pain, stiffness and bladder
problems. ... We urge the courts to deal sympathetically with people with
MS who are charged with cannabis use when seeking relief from their symptoms."
 "Use of cannabis for alleviation of MS symptoms," adopted Aug 2003.

1999: "Scientific data indicate the potential therapeutic value of
cannabinoid drugs, primarily THC, for pain relief, control of nausea and
vomiting, and appetite stimulation. For certain patients, such as
the terminally ill or those with debilitating symptoms, the long-term risks
[associated with smoking] are not of great concern. [Therefore,] clinical
trials of marijuana for medical purposes should be conducted. There
are patients with debilitating symptoms for whom smoked marijuana might provide
relief. Except for the harms associated with smoking, the adverse
effects of marijuana use are within the range of effects tolerated for other
medications."  "Marijuana as Medicine: Assessing the Science Base,"
National Academy Press, 1999.

1998: "We recommend the following actions: The federal
government should re-classify marijuana out of the Schedule 1 category
and allow their prescription where medically appropriate." adopted Nov 15
1998.

1997: "Marijuana looks promising enough to recommend that there be
new controlled studies done. The indications in which varying levels of interest
was expressed are the following: appetite stimulation/cachexia, nausea and
vomiting following anticancer therapy, neurological and movement disorders,
analgesia, [and] glaucoma. Accordingly, the NIH should consider relevant
administrative mechanisms to facilitate grant applications in each of these
areas. Whether or not the NIH is the primary source of grant support for
a proposed bona fide clinical research study, if that study meets U.S. regulatory
standards ... protocol approval, ... the study should receive marijuana."
 "Report to the Director", Workshop on the Medical Utility of Marijuana,
Aug 1997.

2006: "In what could be the first sign of a course reversal by the
National Multiple Sclerosis Society, which has scoffed at medical marijuana
in the past, the group announced this week that it will fund a study on the
effect of marijuana on spasticity in MS patients. While the Society acknowledges
that up to 15% of MS patients use medical marijuana, funding the new study
is the first time the group has indicated it is hearing what those patients
are saying. The society currently rejects the use of marijuana to relieve
MS symptoms. As it notes on its web site, 'Based on the studies to date,
it is the opinion of the National Multiple Sclerosis Society's Medical Advisory
Board that there are currently insufficient data to recommend marijuana or
its derivatives as a treatment for MS. Long-term use of marijuana may be
associated with significant serious side effects. In addition, other well-tested,
FDA-approved drugs are available, such as baclofen and tizanidine, to reduce
spasticity in MS.' The Society said it was moved by inconclusive earlier
studies on the effect of marijuana on MS spasticity to fund a one using a
new measure. The study is not a new one; the group is taking over funding
for ongoing research at the University of California Center for Medicinal
Cannabis Research, which lost funding when the investigation was only partially
completed. The study, by Dr. Mark Agius and fellow researchers at the University
of California-Davis School of Medicine, is scheduled for completion in March
2008." reports
"National
Multiple Scleroisis Society to Fund Study", Drug War Chronilce,
June 23 2006.

1995: "National Nurses Society on Addictions urges the federal government
to remove marijuana from the Schedule 1 category immediately and make
it available for physicians to prescribe. NNSA urges the American Nurses'
Association and other health care professional organizations to support patient
access to this medicine. NNSA supports ongoing human research to determine
alternate active methods of administration to minimize health risks. NNSA
supports research regarding the various cannabinoids and combinations thereof
to determine the greatest therapeutic potential." 
"National Nurses Society
on Addictions' Position Paper: Access to Therapeutic Cannabis", May 1
1995.

2003: "Cannabis has a beneficial effect for many patients. From September
1, 2003 pharmacies can provide medicinal cannabis to patients with a prescription
from a doctor."  Statement of the Health Ministry, reported by Reuters,
Sept 1 2003.

1997: "Federal authorities should rescind their prohibition of the
medical use of marijuana for seriously ill patients and allow physicians
to decide which patients to treat. The government should change marijuana's
status from that of a Schedule I drug ... to that of a Schedule II drug ...
and regulate it accordingly."  editorial by NEJM editor Dr Jerome
Kassirer, Jan 30 1997

2002: "The NJSNA recognizes the therapeutic value and safety of medically
recommended marijuana and ... supports legal access to medically recommended
marijuana for patients in New Jersey who are under the care of a licensed
health care provider."  NJSNA press release, Mar 25 2002.

1997: "NMNA has voted to endorse the concept of allowing for the
therapeutic use of marijuana in a variety of disease states ... when conventional
treatments are ineffective." in a letter from NMNA Pres Ginny Guido to Bryan
A Krumm, RN, BSN, July 28 1997.

2004: "The definitive review of scientific studies ... found medical
benefits related to pain relief, control of nausea and vomiting, and appetite
stimulation. ... While there are a variety of ways of supplying marijuana
for medical use, serious consideration should be given to the 1997 recommendation
... that the FDA reclassify marijuana from Schedule I and provide a consistent,
safe supply."  testimony of Zebulon Taintor, representing the New York
County Medical Society before the New York City Health Committee, Feb 23
2004.

1995: "Marijuana has been found to be effective in the treatment of
glaucoma by reducing intraocular pressure and in reducing nausea and vomiting
caused by chemotherapy. Marijuana has also been effective in stimulating
the appetite of AIDS patients suffering from the wasting syndrome, controlling
spasticity in spinal cord injury patients, and in controlling seizures for
persons suffering from epilepsy and for persons with multiple sclerosis.
...The NYSNA Peer Assistance Committee agrees with the intent and content
of the resolution 'Legalizing Marijuana for Medical Purposes.'"  "Position
Statement on Medicinal Marijuana," passed by the NYSNA Board of Directors,
June 7 1995.

1996: "NCNA urges the Administration and Congress to make cannabis
available as a legal medicine where shown to be safe and effective and to
immediately allow access to therapeutic cannabis through the Investigational
New Drug Program."  "Position Statement on Therapeutic Use of Cannabis,"
adopted by the NCNA, Oct 15 1996.

1994: "... physicians are constantly asked by patients whether or
not marijuana can be used as an adequate or more effective substitute for
dronabinol. As a professional association, we have in various educational
forums addressed this issue by explaining the scientific data upon which
the FDA based its approval of dronabinol. We have also outlined our concerns
over anecdotal side effects of marijuana. However, such warnings to patients
should be based on scientific evidence rather than anecdotal experience.
... Dr. Abrams' study could provide
the data that the medical community needs relative to this subject, and for
that reason PAAC requests that your office support the study with the provision
of the marijuana requested for the study." - Gordon Nary, Executive Director,
in a letter to National Institute on Drug Abuse, Oct. 3, 1994.

"The Medical Society supports H-7588, it is consistent with our belief that
there is sufficient evidence for us to support any physician-patient relationship
that believes the use of marijuana will be beneficial to the patient." 
Steve DeTroy, Director of Government and Public Affairs.

2004: "The Texas Medical Association supports (1) the physician's
right to discuss with his/her patients any and all possible treatment options
related to the patients' health and clinical care, including the use of
marijuana, without the threat to the physician or patient of regulatory,
disciplinary, or criminal sanctions; and (2) further well-controlled studies
of the use of marijuana with seriously ill patients who may benefit from
such alternative treatment."  Resolution of the TMA Council on Scientific
Affairs, adopted Apr 29 2004.

2002: "There is medical value in using marijuana to ameliorate some
symptoms associated with severe illnesses and the treatment thereof. ...
Marijuana is misclassified as a [federal] Schedule I drug and should be
reclassified to permit physicians to prescribe and pharmacies to dispense
medical marijuana."  "Report of the Medical Marijuana Study Committee,"
preliminary report to the Vermont General Assembly, Dec 2002

2003: "VMS current policy on medical marijuana focuses on the need
for additional scientific research, the need for free and open discussion
between physicians and patients and the need to exercise caution in view
of federal criminal penalties for prescribing marijuana or aiding or abetting
patients to violate federal law."  VMS Legislative Bulletin,
Feb 10 2003.

1994: "The Virginia Nurses Association support all reasonable efforts
to end federal policies which prohibit or unnecessarily restrict marijuana's
legal availability for legitimate medical uses; and be it Resolved that the
Virginia Nurses Association provide education to the nurses of Virginia on
the therapeutic use of marijuana and federal prohibition of its use; and
be it Resolved that the Virginia Nurses Association encourage other health
care provider organizations to supp ort medical access to marijuana." 
Resolution passed by the VNA Delegate Assembly, Oct 7 1994.

"Marijuana has helped my symptoms so much that I have become an advocate
for the legalization of medical marijuana for qualified patients like me
 those suffering from debilitating and/or devastatingly painful diseases.
... Because I do not condone breaking any law, I would like to see all 50
states and the federal government decriminalize medical marijuana. I would
also like to see more research into its effects on MS  for the treatment
of pain and spasticity." 
"Taking Action:
Montel on Medical Marijuana & MS Treatment" press release.

1999: "The Wisconsin Nurses Association urges the Governor of Wisconsin
and the Wisconsin Legislature to move expeditiously to make cannabis available
as a legally prescribed medicine where shown to be safe and effective." 
Resolution adopted by WNA, Oct 29 1999.

2001: "The SMS urges the National Institutes of Health (NIH) to implement
administrative procedures to facilitate grant applications and the conduct
of well-designed clinical research into the medical utility of marijuana.
The SMS believes that the NIH should use its resources and influence
to support the development of a smoke-free inhaled delivery system for
marijuana."  SMS Policy Compendium 2000-2001 - Alternative
Medicine.

2003: "The reportedly successful use of cannabis as an alternative
to alcohol, SSRI antidepressants, and stimulants (in
the treatment of ADHD) warrants serious, large-scale investigation. A necessary
first step is for the doctors who are monitoring patients using cannabis
for these purposes to agree on basic definitions, diagnostic criteria, etc.,
and to adopt uniform record-keeping methods. Hergenrathers observation
that half his cannabis-using patients have been able to stop taking
pharmaceutical drugs  and others have reduced their intake  suggests
a line of inquiry that belongs on a common interview form." claims
Fred Gardner from
"Which
Conditions are Californians Actually Treating With Cannabis?",
O'Shaughnessy's Jouurnal of the California Cannabis Research Medical
Group, Summer 2003.

1997: American Medical Association's House of Delegates votes to adopt
a report that recognizes the existence of scientific clinical data showing
cannabis' medical value, urges doctors and patients not be punished for
discussing cannabis as a treatment option, and urges the United States government
to expedite medicinal cannabis research.

1997: "American Medical Association and most other professional medical
bodies do not consider marijuana a safe or effective medicine. Other medical
organizations which oppose the use of smoked marijuana in treatment include
the American Cancer Society, the American Academy of Ophthalmology, the National
Multiple Sclerosis Association [sic], the National Eye Institute, the National
Cancer Institute, the National Institute for Neurological Disorders and Stroke,
and the California Medical Association. ... Fact: No credible medical research
has shown smoked marijuana to be safe, effective, or therapeutically superior
to other substances that have fewer side effects. ... Synthetic
tetrahydrocannabinol, the primary psychoactive ingredient in marijuana, is
currently available in oral form for treatment of HIV Wasting Syndrome and
chemotherapy-induced nausea. A double-blind study confirmed that this synthetic
drug was preferred by chemotherapy patients by an almost two-to one margin.
Controlled research studies are needed to ... determine if [marijuana] has
a legitimate medical use. To this end, ONDCP has committed $965,000 to the
Institutes of Medicine for a comprehensive review of existing literature
for medical uses of marijuana." claims "Marijuana: Myths and Truth", US Office
of National Drug Control Policy.(seeParents
Ending Prohibition's Rebuttal,
Patients
Out of Time's Rebuttal)

1997: "With drug use among our children on the upswing, the last message
we need to send our youth is that smoked marijuana is a safe, effective
medicine." claims "Report on Legalization Trends", US Office of National
Drug Control Policy, Feb, 7, 1997.

1997: "... there is no one reliable study that demonstrates marijuana
has any medicinal value. ... In 1994, a U.S. Court of Appeals ... noted that
marijuana's medicinal value has never been proven in sound scientific studies."
claims US Drug Enforcement Administration.

1997: "American Medical Association and most other professional medical
bodies do not consider marijuana a safe or effective medicine. ... Fact:
No credible medical research has shown smoked marijuana to be safe, effective,
or therapeutically superior to other substances that have fewer side effects."
claims "Marijuana: Myths and Truth", US Office of National Drug Control Policy.
(seePatients
Out of Time's Rebuttal)

1997: "With drug use among our children on the upswing, the last message
we need to send our youth is that smoked marijuana is a safe, effective
medicine." claims "Report on Legalization Trends", US Office of National
Drug Control Policy, Feb, 7, 1997.

Mouth

2008: "Cannabis smoking may be a risk factor for periodontal disease
that is independent of the use of tobacco. ... Three
cannabis exposure groups were determined: no exposure (293 individuals, or
32.3%), some exposure (428; 47.4%), and high exposure (182; 20.2%). At age
32 years, 265 participants (29.3%) had 1 or more sites with 4 mm or greater
CAL [periodontal combined attachment loss], and 111 participants (12.3%)
had 1 or more sites with 5 mm or greater CAL. Incident attachment loss between
the ages of 26 and 32 years in the none, some, and high cannabis exposure
groups was 6.5%, 11.2%, and 23.6%, respectively. After controlling for tobacco
smoking (measured in pack-years), sex, irregular use of dental services,
and dental plaque, the relative risk estimates for the highest cannabis exposure
group were as follows: 1.6 (95% confidence interval [CI], 1.2-2.2) for having
1 or more sites with 4 mm or greater CAL; 3.1 (95% CI, 1.5-6.4) for having
1 or more sites with 5 mm or greater CAL; and 2.2 (95% CI, 1.2-3.9) for having
incident attachment loss (in comparison with those who had never smoked
cannabis). Tobacco smoking was strongly associated with periodontal disease
experience, but there was no interaction between cannabis use and tobacco
smoking in predicting the condition's occurrence." claims W Murray Thomson,
et al,
"Cannabis
Smoking and Periodontal Disease Among Young Adults", Journal of Amercian
Medical Association, Feb 6 2008. Also summarized in
"Smoking
marijuana associated with increased risk for gum disease",
"Cannabis
indicated as possible risk for gum disease in young people"

Multiple Sclerosis

2006: "Tysabri has been linked to a potentially fatal brain infection
called progressive multifocal leukoencephalopathy, or PML. The drug's
manufacturers voluntarily pulled it from the market last year, following
the deaths of two patients. The drug had been sold for just four months.
Dozens of multiple sclerosis patients told a Food and Drug Administration
advisory committee Tuesday that they should be allowed to choose whether
to take Tysabri. ... In statements frequently punctuated by sobbing pleas,
patients told the Peripheral and Central Nervous System Drugs advisory committee
that MS posed an even greater risk than did PML. ... Biogen Idec and Elan
withdrew Tysabri from the market in February 2005 after two patients in clinical
trials involving 7,000 people died of PML." reports Associated Press
"FDA
panel mulls rare reversal on MS drug", Mar 8 2006

2005: "Health Canada's approval of Sativex was based on the results
of a four-week clinical trial involving 66 patients with MS-related neuropathic
pain that was carried out in Great Britain, in which half received Sativex
and the other half received a placebo. The results showed participants used
Sativex (prescribed on an as-needed basis) less often compared to the controls
using placebo. Sativex is administered via a spray into the mouth, which
is well suited to the variable nature of neuropathic pain experienced by
people with MS. Placebo patients in the study also used a spray. The Sativex
group reported pain relief, less sleep disturbance and felt their condition
had improved. But they also experienced more dizziness, nausea and fatigue.
... Sativex isolates the cannabinoid components, delta-9-tetrahydrocannabinol
(THC) and cannabidiol (CBD), representing only two of the more than 60 related
chemicals that make up the marijuana plant. It is believed that THC helps
patients with pain while CBD has a neurological effect, and that isolating
these two cannabinoids will enable patients to eliminate many of the side-effects
that are associated with the use of medical marijuana." reports David Hodges,
"Pot-based
drug shows promise for neuropathic pain", Medical Post vol 41
issue 19, May 17 2005.

2004: "Cannabis may loosen the stiff and spastic muscles of multiple
sclerosis sufferers, and not just their minds, a follow-up study has found.
The results contradict findings from the first phase of the study,
where improvements seemed to be largely due to 'good moods'. 'There does
seem to be evidence of some benefit from cannabis in the longer term that
we didnt anticipate in the short term study,' says John Zajicek, at
Peninsula Medical School in Exeter, UK, and one of the research team. In
2003, Zajicek and his colleagues published results on the largest study to
date of cannabinoids and MS. The trial included 630 advanced-stage MS patients
who took either cannabinoid compounds or a placebo for 15 weeks. Compared
with those on placebos, patients who received active compounds said they
both felt less pain and less muscle spasticity  the spasms characteristic
of this neurodegenerative disease. ... When the short-term study ended, however,
the researchers gave all subjects the opportunity to continue their treatment
for a full year. ... More than 500 patients agreed to stay on their original
treatment. One group took pills of D9-tetrahydrocannabinol (THC), the active
ingredient in cannabis. The second group received natural cannabis extract,
and the third group took a placebo. At the end of the 12 month period, the
patients were evaluated again using the same measures as in the first study.
But this time, physiotherapists saw a marked improvement for subjects on
active drugs. They had reduced muscle spasticity and an improved overall
score for their level of disability. ... the results do support animal research
that shows cannabinoids may slow nerve cell death and protect against damage.
The findings were presented at the British Association for the Advancement
of Science Festival, in Exeter, UK." reports Anna Gosline from
"Cannabis truly
helps multiple sclerosis sufferers", New Scientist, Sept 10 2004.

2004: "Diagnosed with MS in 2001, [Matthew] Barber said he has exhausted
all of the acceptable, and expensive, forms of treatment for a disease that
affects the central nervous system and has left lesions on Barber's brain.
Barber said without the marijuana, he has pain and spasms, imbalance, dizziness,
the loss of leg function and sometimes even blindness. Barber, who
served in the Army during the first Gulf War, said a neurologist through
Veterans Affairs told him that because all other treatments have failed,
that marijuana may alleviate some symptoms." reports Ian C Storey from
"MS
Sufferer Vows To Fight Pot Laws", Traverse City Record-Eagle,
July 7 2004.

2004: "Daytime television talk show host Montel Williams threw his
support Tuesday behind legalizing medical marijuana in New York, saying pot
helps him cope with multiple sclerosis. Williams, who was diagnosed with
the debilitating neurological disease in 1999, said he uses marijuana every
night before bed to relieve the pain in his legs and feet. 'I'm breaking
the law every day, and I will continue to break the law,' said a defiant
Williams, flanked by state lawmakers and health officials, who are lobbying
to make pot legal for medicinal purposes. The Emmy award-winning host of
the nationally syndicated Montel Williams Show, recalled how prescription
painkillers and even morphine failed to control his
tremors and spasms. Williams said it was not until he started using marijuana
that he was able to feel like a 'contributing member of society.' " reports
Alicia Chang from
"Montel
Williams Pushes Pot  for Medical Relief", Associated Press, May
4 2004.

2004: "... I tried several commonly prescribed painkillers. The results?
Little relief and unbearable side effects. The last alternative left? Medical
marijuana. In fact, marijuana has helped my symptoms so much that I have
become an advocate for the legalization of medical marijuana for qualified
patients like methose suffering from debilitating and/or devastatingly
painful diseases. ... Because I do not condone breaking any law, I would
like to see all 50 states and the federal government decriminalize medical
marijuana. I would also like to see more research into its effects on
MSfor the treatment of pain and spasticity." claims
Montel Williams from
"Taking
Action: Montel on Medical Marijuana & MS Treatment", Montel Williams
MS Foundation, 331 W 57th St #420, New York, NY 10019,
montelms.org, email
msfoundation@montelshow.com

2003: "Treatment with [Marinol] cannabinoids did not have a beneficial
effect on spasticity when assessed with the Ashworth scale. However, though
there was a degree of unmasking among the patients in the active treatment
groups, objective improvement in mobility and patients' opinion of an improvement
in pain suggest [Marinol] cannabinoids might be clinically useful." claims
John Zajicek, Patrick Fox, Hilary Sanders, David Wright, Jane Vickery, Andrew
Nunn, Alan Thompson, "Cannabinoids for treatment of spasticity and other
symptoms related to multiple sclerosis (CAMS study): multicentre randomised
placebo-controlled trial",
The Lancet,
vol 362, no 9395, Nov 2003.thelancet.com/journal/vol362/iss9395/full/llan.362.9395.original_research.27670.1,
cannabisnews.com/news/thread17744.shtml

2003: "This is an exciting time for cannabinoid research. There is
a growing amount of data to suggest that cannabis (marijuana) can alleviate
symptoms like muscle spasticity and pain in patients with MS. ... cannabinoids
are not known to cause deaths by direct toxicity ... Given the favorable
effects observed in animal studies, the immunosuppressive and neuroprotective
potential of cannabinoids, and anecdotal reports from MS patients claiming
that cannabis use reduces the frequency of their MS attacks, some authors
believe that cannabinoids could be used to alter the underlying course of
the disease."  "Cannabis Use in Multiple Sclerosis: Excited Interest",
Canadian Journal
of Neurological Sciences, Aug 2003, pgs 181-182.cjns.metapress.com/app/home/content.asp?wasp=c5v8d08eqpdvtg91ty47&referrer=contribution&format=3&page=1&pagecount=2

2003: "The majority of respondents (96%) was aware cannabis was
potentially therapeuticallyuseful for MS and most (72%) supported legalization
for medicinal purposes. ... Symptoms reported to be ameliorated included
anxiety/depression, spasticity and chronic pain. ... Conclusions: Subjective
improvements in symptom experience were reported by the majority of people
with MS who currently use cannabis. Further evaluation of this substance
is warranted." claims Page SA, Verhoef MJ, Stebbins RA, Metz LM, Levy JC,
"Cannabis use as described by people with multiple sclerosis.",
Canadian Journal
of Neurological Sciences, Aug 2003, pgs 201-205.

2002: "There is a growing amount of evidence to suggest that cannabis
and individual cannabinoids may be effective in suppressing certain symptoms
of multiple sclerosis and spinal cord injury, including spasticity and pain.
... Clinical trials have shown that cannabis, Delta(9)-tetrahydrocannabinol,
and nabilone can produce objective and/or subjective relief from spasticity,
pain, tremor, and nocturia in patients with multiple sclerosis (8 trials)
or spinal cord injury (1 trial). The clinical evidence is supported by results
from experiments with animal models of multiple scleroisis." claims Pertwee
RG, "Cannabinoids and multiple sclerosis.", Pharmacological
Therapeutics, Aug 2002, pgs 165-174.

2002: "The neuroprotective effect of cannabinoids may have potential
clinical relevance for the treatment of neurodegenerative disorders such
as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson.s
disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and
Patrick Weydt from
"Cannabis:
Old medicine with new promise for neurological disorders"

2000: "The exacerbation of these signs after antagonism of the CB1
and CB2 receptors, notably the CB1 receptor, using SR141716A and SR144528
indicated that the endogenous cannabinoid system may be tonically active
in the control of tremor and spasticity. This provides a rationale for patients'
indications of the therapeutic potential of cannabis in the control of the
symptoms of multiple sclerosis ..." claims Baker D, Pryce G, Croxford JL,
Brown P, Pertwee RG, Huffman JW, Layward L, "Cannabinoids control spasticity
and tremor in a multiple sclerosis model.", Nature, Mar 2000, pgs
84-87.

1989: "All animals treated with placebo developed severe clininical
EAE [experimental autoimmune encephalomyelitis] 10-12 days post-injection
(dpi) and more than 98% died by 15 dpi. THC-treated animals had either no
clinical signs or mild signs with delayed onset (13-15 dpi) with survival
greater than 95%. Examination o f central nervous system tissue revealed
a marked reduction of inflammation in the THC-treated animals. Therefore,
as THC has been shown to inhibit both clinical and histologic EAE, it may
prove to be a new and relatively innocuous agent for the treatment of
immune-mediated diseases." claims Lyman WD, Sonett JR, Brosnan CF, Elkin
R, Bornstein MB, "Delta 9-tetrahydorcannabinol: a novel treatment for
experimental autoimmune encephalomyelitis.", Journal of Neuroimmunology,
Jun 1989, pgs 73-81.

1989: "The chronic motor handicaps of a 30-year-old multiple sclerosis
patient acutely improved while he smoked a marihuana cigarette. ... It is
concluded that cannabinoids may have powerful beneficial effects on both
spasticity and ataxia that warrant further evaluation." claims Meinck HM,
Schonle PW, Conrad B, "Effect of cannabinoids on spasticity and ataxia in
multiple sclerosis.", Journal of Neurology, Feb 1989, pgs 120-122.

1987: "At doses greater than 7.5 mg [of THC] there was significant
improvement in patient ratings of spasticity compared to placebo. These positive
findings in a treatment failure population suggest a role for THC in the
treatment of spasticity in multiple sclerosis." claims Ungerleider JT, Andyrsiak
T, Fairbanks L, Ellison GW, Myers LW, "Delta-9-THC in the tratment of spasticity
associated with multiple sclerosis.", Adv Alcohol Substance Abuse,
1987, pgs 39-50.

1986: "Cannabis", Therapeutic Claims in Multiple Sclerosis,
published by International Federation of Multiple Sclerosis, pg 226.

1981: "For the group, 10 mg THC significantly reduced spasticity by
clinical measurement (P less than 0.01). Quadiceps EMG interference pattern
was reduced in those four patients with primarily extensor spasticity. THC
was administred to eight other patients with spasticity and other CNS lesions.
Responses varied, but benefit was seen in three of three patients with 'tonic
spasms.' " claims Petro DJ, Ellenberger C Jr, "Treatment of human spasticity
with delta 9-tetrahydorcannabinol.", Journal of Clinical Pharmacology,
Aug-Sept 1981, pgs 413S-416S.

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ...
My neurologist prescribed the drugs Compazine and Antivert. They had little
affect on the nausea and no affect on the appetite, even after the dosage
was doubled. After a couple of weeks of feeling sick and not eating, I had
lost 15 pounds and no medication was helping. ... I decided to try smoking
Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke
were gone I began to relax and get an appetite. I could finally eat again.
Since that time, I have used cannabis to maintain a healthy body weight and
a decent standard of living. For years I left my prescription drugs setting
on the counter, as Cannabis was more effective." cliams John E Precup from
"Patient
Testimonials"

"I have Multiple Sclerosis and have been able to receive little to no relief
from the FDA approved medicines my doctors recommended. The doctors had me
on Ritalin to give me energy and Prozac to keep my moods level. I took Vicodin
[hydrocodone and
acetaminophen] and Soma to help with pain. I
had to learn to give myself shots, so that I could take my Copaxone drug
... I am not taking any of those drugs now, I haven't for four years now
I have been smoking medical marijuana. Since I have been medicating my body
with marijuana I have never felt better, my disease has mostly gone into
remission ... I am able to work part time and that was not something that
was thought possible four short years ago. Marijuana has changed my life
with the best possible thing - Hope." claims Meagan Boyd from
"Patient
Testimonials".

Nail Patella Syndrome (NPS)

1989: "I am one of only 34 known medically ill individuals who have
been approved to use marijuana legally in the U.S. I suffer from a rare
neurological disease known as Nail Patella Syndrome (NPS). There are only
200 known cases of this genetic disorder. Of those, eight percent are affected
with organ and immune system complications which kills most of them by the
age of 40 ... I had a lifetime of mysterious pain and physical ailments ...
marijuana was effective in treating the chronic pain associated with my
condition. I was born with mild deformities including missing fingernails,
double jointed fingers, poorly jointed elbows, and small knee caps." claims
George McMahon, from "My Story"
chiana.trvnet.net/~mmcmahon/mystory.htm

Nausea

1999: "In 1992 I was found to have testicular cancer. My chemotherapy
put me in the hospital for five days at a time, once a month, for four months.
But midway through my treatment I could tell that Zofran, then a hot new
drug prescribed to combat nausea, was losing its effect. For the remainder
of my chemotherapy I turned to marijuana to keep my head out of the toilet.
None of the doctors or nurses at the hospitals I went to for treatment (New
York University Medical Center) or consultation (Memorial Sloan-Kettering)
discouraged me from using marijuana should the need arise. They said they
had patients who had benefited from it when other drugs had failed." claims
Richard Brookhiser, senior
editor of National Review, from a letter to New York Times,
May 22, 1999.

1988: "Marijuana cigarettes in many cses are superior to synthetic
THC capsules in
reducing chemotherapy-induced nausea and
vomiting. Marijuana cigarettes have an important, clear advantage over synthetic
THC capsules in that natural marijuana is inhaled and generally takes effect
more quickly than the synthetic capsule" claims
Francis L Young, Chief Administrative
Law Judge, US Drug Enforcement Administration, 1988.

1988: "Patient evaluations have indicated that approximately ninety-three
(93) percent of marijuana inhalation treatment episodes are reported to be
'effective' or 'highly effective' when compared to other antiemetics." 78%
of 56 patients had no improvement with standard antiemetics, claims Vinciguerra,
et al, "Inhalation Marijuana as an Antiemetic for Cancer Chemotherapy", New
York State Journal of Medicine, pgs 525-527, Oct 1988.

1986: "I started feeling the changes pretty much right away. Smoking
marijuana also felt ten times better than taking Marinol
pill. It helped reduce my nausea and I could hold down food better." claims
Jim Kerns, cancer and
chemotherapy patient.

1983: "We found both marijuana smoking and THC capsules to be effective
antiemetics. We found an approximate 23 percent higher success rate among
those patients smoking (90%) than among those administered THC capsules (67%).
... We found that the major reason for smoking failure was smoking intolerance;
while the major reason for THC capsule failure was nausea and vomiting so
severe that the patient could not retain the capsule." claims Annual Report:
Evaluation of Marijuana and Tetrahydrocannabinol in the Treatment of Nausea
and/or Vomiting Associated with Cancer Therapy Unresponsive to Conventional
Anti-Emetic Therapy: Efficacy and Toxicity, Board of Pharmacy, State
of Tennessee, July 1983.

1981: 71% of patients randomized to receive cannabis report no emesis
to moderate nausea. 90% of patients receiving cannabis choose to remain on
cannabis rather than switch to the antiemetic Torecan, 95% of patients randomized
to Torecan choose to discontinue use of Torecan and switched to cannabis,
claims "Michigan Department of Public Health Marijuana Therapeutic Research
Project, Trial A 1980-81", Department of Social Oncology, Evaluation Unit,
Michigan Cancer Foundation, March 18, 1982.

1981: "74 percent of the cancer patients treated in the program have
reported that [inhaled] marijuana is more effective in relieveing their nausea
and vomiting than any other drug they have tried." claims California Research
Advisory Panel, Annual Report of the California Research Advisory Panel,
vol 12, submitted to the Governor and Legislature.

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ...
My neurologist prescribed the drugs Compazine and Antivert. They had little
affect on the nausea and no affect on the appetite, even after the dosage
was doubled. After a couple of weeks of feeling sick and not eating, I had
lost 15 pounds and no medication was helping. ... I decided to try smoking
Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke
were gone I began to relax and get an appetite. I could finally eat again.
Since that time, I have used cannabis to maintain a healthy body weight and
a decent standard of living. For years I left my prescription drugs setting
on the counter, as Cannabis was more effective." cliams John E Precup from
"Patient
Testimonials"

2013: "A new study from Harvard University may help dismiss concerns about the link between marijuana use and schizophrenia.
While many still debate the potential for marijuana to cause schizophrenia, researchers at Harvard Medical School say there has
'yet to be conclusive evidence that cannabis use may cause psychosis.' Their latest study, published last week in the journal Schizophrenia Research,
adds support to the role of genetic factors in schizophrenia, and that marijuana use alone does not increase the risk of developing the disorder.
'In summary, we conclude that cannabis does not cause psychosis by itself. In genetically vulnerable individuals,
while cannabis may modify the illness onset, severity and outcome, there is no evidence from this study that it can cause the psychosis.'
The team, led by Lynn DeLisi, MD, Professor of Psychiatry at Harvard Medical School, compared the family histories of
108 schizophrenia patients and 171 individuals without schizophrenia to determine whether cannabis use was a factor in developing the disorder.
They found that a family history of schizophrenia increased the risk of developing schizophrenia,
regardless of whether or not an individual used cannabis. The authors say further studies should investigate whether marijuana can interact with
genetic factors to affect the age at which schizophrenia develops. However, the latest findings provide enough evidence for
Dr. DeLisi and her team to conclude that cannabis 'is unlikely to be the cause of illness.' ""Marijuana Does Not Cause Schizophrenia, Harvard Study Finds"
by Leaf Science, Dec 8 2013

2005: "Can smoking pot make you potty? Even as the UK government mulls
over evidence that cannabis can cause mental health problems, a new study
suggests the link may be hazier than thought. ... Some studies have suggested
long-term cannabis use can increase your risk of developing schizophrenia
(New Scientist, 26 March 2005, p 44). Others have linked the drug
to milder 'schizotypal traits' that include odd, magical beliefs and social
paranoia. To test whether people who already have these traits are more likely
to start using cannabis, Jason Schiffman at the University of Hawaii in Honolulu
and his colleagues gave 189 students questionnaires about their cannabis
use. The students were also asked if they had any schizotypal traits and
if so when these traits first arose. The results showed that the majority
of people who'd recently used cannabis had schizotypal symptoms before using
the drug (Psychiatry Research, vol 134, p 37). Schiffman admits that
the limited study 'leaves far more questions than answers' - for instance,
it gives no clues as to why people with such traits might be attracted to
cannabis." 
"Cannabis
and schizophrenia link blurs further", New Scientist, Apr 16 2005.

2002: "The neuroprotective effect of cannabinoids may have potential
clinical relevance for the treatment of neurodegenerative disorders such
as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson's
disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and
Patrick Weydt from
"Cannabis:
Old medicine with new promise for neurological disorders"

Neuropathy

2001: "I have been a diabetic for 25 of those years. During this time,
I have had amputations to both feet. I've also had a stroke and am on dialysis.
I have what is called neuropathy. This is a highly painful nerve disorder.
Sometimes the pain was so severe I would wish my hands were cut off. I was
taking 2800mg of Neuroten a day plus 4 to 6 Percocet. I also have severe
hypertension and take 100 mg of Zoloft. After two years I became so dependent
on the Percocet. I was taking sometimes more than 10 a day. Then I started
smoking marijuana. It helped me stop taking the narcotics. I have stopped
taking Percocet and take only 400mg of the Neuroten. My pain is gone. When
I get really hyper I take about three hits and stay calm for hours. This
dialysis really zaps your energy. But I take a few hits after treatment,
and have energy to function all day." claims anonymous patient from
"Patient
Story - Neuropathy", May 6 2001, updated July 19 2001.

Obsessive Compulsive Disorder (OCD)

2001: "I have smoked weed off and on for 20 years, and now everyday.
I find that with it I take less Paxil, and I am able to function better.",
Manic-depression/obsessive compulsive disorder patient, Mar 11 2001.

2003: "Treatment with [Marinol] cannabinoids did not have a beneficial
effect on spasticity when assessed with the Ashworth scale. However, though
there was a degree of unmasking among the patients in the active treatment
groups, objective improvement in mobility and patients' opinion of an improvement
in pain suggest [Marinol] cannabinoids might be clinically useful." claims
John Zajicek, Patrick Fox, Hilary Sanders, David Wright, Jane Vickery, Andrew
Nunn, Alan Thompson, "Cannabinoids for treatment of spasticity and other
symptoms related to multiple sclerosis (CAMS study): multicentre randomised
placebo-controlled trial",
The Lancet,
vol 362, no 9395, Nov 2003.thelancet.com/journal/vol362/iss9395/full/llan.362.9395.original_research.27670.1

2003: "This is an exciting time for cannabinoid research. There is
a growing amount of data to suggest that cannabis (marijuana) can alleviate
symptoms like muscle spasticity and pain in patients with MS. ... cannabinoids
are not known to cause deaths by direct toxicity ... Given the favorable
effects observed in animal studies, the immunosuppressive and neuroprotective
potential of cannabinoids, and anecdotal reports from MS patients claiming
that cannabis use reduces the frequency of their MS attacks, some authors
believe that cannabinoids could be used to alter the underlying course of
the disease."  "Cannabis Use in Multiple Sclerosis: Excited Interest",
Canadian Journal
of Neurological Sciences, Aug 2003, pgs 181-182.cjns.metapress.com/app/home/content.asp?wasp=c5v8d08eqpdvtg91ty47&referrer=contribution&format=3&page=1&pagecount=2

2003: "The majority of respondents (96%) was aware cannabis was
potentially therapeuticallyuseful for MS and most (72%) supported legalization
for medicinal purposes. ... Symptoms reported to be ameliorated included
anxiety/depression, spasticity and chronic pain. ... Conclusions: Subjective
improvements in symptom experience were reported by the majority of people
with MS who currently use cannabis. Further evaluation of this substance
is warranted." claims Page SA, Verhoef MJ, Stebbins RA, Metz LM, Levy JC,
"Cannabis use as described by people with multiple sclerosis.",
Canadian Journal
of Neurological Sciences, Aug 2003, pgs 201-205.

1997: "... researchers reported Sunday that active chemicals found
in the [cannabis] plant could serve as an effective remedy for the millions
who suffer serious pain each year, without the unwanted side effects of more
traditional morphine-like drugs." reports Robert Lee
Hotz from
"Marijuana
for pain relief?", Los Angeles Times, Oct 27 1997.

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and
acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium to control the depression associated with
his constant turmoil. There are occasions when he is seen in the office or
the emergency room and given shots of Demerol [meperidine] and Phenergren
[promethazine]. Even these shots do not give him full relief of his headaches,
but do, when things are severe, give him a few hours of peace. The only
drug that seems to give William any true felief from pain is that from
smoking marijuana. ... Having seen him in constant pain without the availability
of the Marinol or marijuana purchased from a street dealer, I have no question
that there is pain relief afforded to him by the drug. It should be noted
that the Marinol only gives him partial and inadequate pain relief." claims
Dr Michael E Mayle, DO, in a letter to Whom It May Concern, 1996.

1989: "I am one of only 34 known medically ill individuals who have
been approved to use marijuana legally in the U.S. I suffer from a rare
neurological disease known as Nail Patella Syndrome (NPS). There are only
200 known cases of this genetic disorder. Of those, eight percent are affected
with organ and immune system complications which kills most of them by the
age of 40 ... I had a lifetime of mysterious pain and physical ailments ...
marijuana was effective in treating the chronic pain associated with my
condition. I was born with mild deformities including missing fingernails,
double jointed fingers, poorly jointed elbows, and small knee caps." claims
George McMahon, from "My Story"
chiana.trvnet.net/~mmcmahon/mystory.htm

2004: "The long-term treatment of Parkinson disease (PD) may be
complicated by the development of levodopa-induced dyskinesia. Clinical and
animal model data support the view that modulation of cannabinoid function
may exert an antidyskinetic effect. The authors conducted a randomized,
double-blind, placebo-controlled crossover trial to examine the hypothesis
that cannabis may have a beneficial effect on dyskinesia in PD. ... Cannabis
was well tolerated, and had no pro- or antiparkinsonian action. There was
no evidence for a treatment effect on levodopa-induced dyskinesia as assessed
by the UPDRS, or any of the secondary outcome measures. CONCLUSIONS: Orally
administered cannabis extract resulted in no objective or subjective improvement
in dyskinesias or parkinsonism." 
"Cannabis
for dyskinesia in Parkinson disease: a randomized double-blind crossover
study" by Carroll, Bain, Teare, Liu, et al, Neurology, #63(7), Pgs 1245-1250,
Oct 12 2004.

2002: "The neuroprotective effect of cannabinoids may have potential
clinical relevance for the treatment of neurodegenerative disorders such
as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson's
disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and
Patrick Weydt from
"Cannabis:
Old medicine with new promise for neurological disorders"

Polio

Includes post polio syndrome

"... a chronic fatigue/fibromyalgia support group recommended marijuana ...
for [my] post polio syndrome. I was amazed. Just a few puffs took away the
pain. I was able to move around comfortably to walk, clean my house, and
do all the things I needed to do. While living in California, and then for
awhile in Hawaii, I had legal access to marijuana. This was during the time
after these states had made marijuana available for medical use. ... I returned
to Arkansas ... Since my return, I have not been able to obtain marijuana.
My doctor has prescribed a variety of medications but these seem to have
little effect on my symptoms. I still feel stiff and my body aches. The worst
part is that these drugs make me very groggy. I'm afraid to drive and I don't
feel very sociable. ... I don't know how much these powerful pain medications
may be contributing to my depression, but now I'm also having to take strong
mood altering drugs to control the depression. I take Darvocet for pain,
Flexeril for muscle spasms, Doxipin [dibenzoxepin] for pain and as a sedative,
Celexa for depression, and Klonopin as an antidepressant. ... I am seriously
considering moving to one of the states where marijuana is available ..."
claims Jean Cooper from
"Patient
Story - Jean - Childhood Polio".

Polls

2005: 78% of Americans support "making marijuana legally available
for doctors to prescribe in order to reduce pain and suffering", reports
Gallup, Nov 2005.

2004: "The majority of respondents 45 and older (72%) agree that adults
should be allowed to legally use marijuana for medical purposes if a physician
recommends it. ... More than one-half of respondents believe that marijuana
has medical benefits (59%) and that they would obtain marijuana for a suffering
loved one (55%). One-third of respondents think that adults should be allowed
to grow marijuana for medical purposes (33%) and one-quarter (23%) think
that marijuana should be legalized. Three-quarters of respondents think that
marijuana is addictive (74%) and almost one-third (30%) have smoked marijuana.The
majority of respondents think that the decision to legalize marijuana is
a federal issue (52%). ... More respondents from the north east (79%) and
west (82%) agreed that adults should be allowed to legally use marijuana
for medical purposes compared to respondents from other areas of the country.
Respondents from the west (69%) were more likely to agree that marijuana
has medical benefits compared to their counterparts. More respondents from
the north east (60%), and from the west (62%) said they would obtain marijuana
for a suffering loved one. Respondents from the west (41%) were also more
likely to agree adults should be allowed to grow marijuana for medical purposes
compared to their counterparts. The percentage of respondents who believe
all marijuana use should be legalized did not vary significantly across different
areas of the country. However, respondents from the west (49%) were more
likely to think the decision to legalize marijuana should be a state issue
compared to other respondents (38% overall)." reports Jean Kalata from
"Medical
Uses of Marijuana: Opinions of U.S. Residents 45+" (PDF),
AARP The
Magazine, Dec 2004. Also seeHTML
summary

1999: 96 percent of respondents said they support the use of cannabis
for medicinal purposes, 89 percent of respondents said they did not think
legalizing medical cannabis would open the doors to the legalization of other
illicit drugs, reports CNN Interactive, Apr 1999.

Potency

2006: "Cannabinoid content of NIDA pot is highly variable, and a THC
potency of 6 to 8 percent is about as high as researchers can hope for. By
contrast, Canada distributes medical marijuana to patients at 12.5 percent,
and medical marijuana in the Netherlands ranges from 13 to 18 percent potency.
'I've spoken to patients who have used [NIDA marijuana], and they've said
it's everything from worthless to other descriptions I should not use,' [Lyle
E] Craker says. 'The patient has to smoke one cigarette after the other to
get any effective relief from pain.' Ethan Russo, a neurologist and now a
senior medical adviser to GW Pharmaceuticals, conducted patient studies with
NIDA marijuana and reported, 'A close inspection of the contents of NIDA-supplied
cannabis cigarettes reveals them to be a crude mixture of leaf with abundant
stem and seed components. ... The resultant smoke is thick, acrid, and
pervasive.' " reports Jessica Winter,
"Weed Control",
Boston Globe, May 28 2006. Also see ;US
NIDA, Lyle E Craker,
Ethan Russo

2004: "The Marijuana Potency Project, at the University of Mississippi,
analysed more than 30,000 samples seized over the past 18 years by the
authorities. It found that the average level of the active ingredient in
marijuana, tetrahydrocannabinol (THC), jumped from 3.5 per cent in 1985 to
more than 7 per cent in 2003." reports Richard Luscombe from "Bush Targets
Marijuana Smokers", Observer UK, July 25 2004.

2002: "Parents are often unaware that today's marijuana is different
from that of a generation ago, with potency levels 10 to 20 times stronger
than the marijuana with which they were familiar." claims US Office of National
Drug Control Policy Director John P
Walters,
"The
Myth of 'Harmless' Marijuana", Washington Post, May 1 2002, pg
A25.

2002: "Federal research shows that the average potency of cannabis
in the US has increased very little. According to the federal Potency Monitoring
Project, in 1985, the average THC content of commercial-grade marijuana was
2.84%, and the average for high-grade sinsemilla in 1985 was 7.17%. In 1995,
the potency of commercial-grade marijuana averaged 3.73%, while the potency
of sinsemilla in 1995 averaged 7.51%. In 2001, commercial-grade marijuana
averaged 4.72% THC, and the potency of sinsemilla in 2001 averaged 9.03%."
 Quarterly Report #76, Nov. 9, 2001-Feb. 8, 2002, Table 3, pg
8, University of Mississippi Potency Monitoring Project (Oxford, MS: National
Center for the Development of Natural Products, Research Institute of
Pharmaceutical Sciences, 2002), Mahmoud A. ElSohly, PhD, Dir, NIDA Marijuana
Project (NIDA Contract #N01DA-0-7707).

1999: "According to University of Mississippi analyses, the THC content
of commercial-grade marijuana has risen slowly over the years from an average
of 3.71 percent in 1985 to an average of 5.57 percent in 1998. These analyses
also show a corresponding rise in sinsemilla THC content from 7.28 percent
in 1985 to 12.32 percent in 1998." More recently, the US National Drug
Intelligence Center's "National Drug Threat Assessment 2002 " report, released
December 2001, stated that "Overall, potency, as characterized by THC content,
is still increasing. According to data from the Potency Monitoring Project,
the THC content of commercial-grade marijuana increased from 1997 to 2000
for commercial-grade (4.25% to 4.92%) and for sinsemilla (11.62% to 13.20%)."
 "Drug Intelligence Brief: The Cannabis Situation in the United States,
December 1999"

1997: "Marijuana is currently up to 25 times more potent than it was
in the 1960's ..." claims Say It Straight: Our Health, Our Youth and
Marijuana, Community Anti-Drug Coalitions of America.

1991: "The repetition of undocumented potency claims by governmental
and governmentally funded speakers parallels the similarly undocumented claims
of marijuana's adverse ... effects." claims
John P Morgan, MD, in a letter published
in New York Times, Nov 19, 1991.

1980: "Marijuana is up to ten times more potent than that smoked a
decade ago."  "Marijuana: The Myth of Harmlessness Goes Up in Smoke",
Saturday Evening Post, Jul/Aug 1980, pg 34.

"It appears that Mr Walters is given
to histrionics, or of simply being at best ingenuous, at worst a bald-faced
liar. Clearly, significantly powerful cannabis preparations have been available
for decades. If we narrow our focus to just 'marijuana,' the lowest recorded
average potency was measured in 1973 at 0.83 percent THC. By contrast, the
highest recorded average potency for 'marijuana' was measured in 2001 at
4.72 percent THC. These numbers indicate that today's 'marijuana' weighs
in at less than 6 times as potent as that from the last generation." claims
Brian C Bennett from
"Modern
Day 'Super Weed'"

Pregnancy

2013: "After evaluating the children at 3 days old, one month old, four years old, and five years old,
[Melanie C] Dreher found no adverse effects among the marijuana-exposed group, even with the babies of heavy users.
In fact, at the one-month evaluation, the children of mothers who smoked pot performed better on every variable studied,
and were less prone to stress-related anxiety  findings Dreher attributed to the higher social standing of the
moms who could afford ganja." reports M J Dylan from "Pot and Pregnancy: It’s Harmless, So Why Are Moms Still Prosecuted?"Opposing Views, Sept 10 2013

2010: "Warnings that marijuana causes birth defects date back to the late 1960s.
Some researchers claimed to have found chromosomal abnormalities in blood cells taken from marijuana users.
They predicted that young men and women who used marijuana would produce deformed babies.
Although later studies disproved this theory, some current drug education materials still claim that
genetic damage is passed on by marijuana users to their children. ...
Dozens of studies have compared the newborn babies of women who used marijuana during pregnancy with the
babies of women who did not. Mainly, they have looked for differences in birth weight, birth length,
head circumference, chest circumference, gestational age, neurological development, and physical abnormalities.
Most of these studies, including the largest study to date with a sample of over twelve thousand women, have found
no differences between babies exposed to marijuana prenatally and babies not exposed.
Given the large number of studies and the large number of measures, some differences are likely to occur by chance.
Indeed, researchers have found differences in both directions. In some studies, the babies of marijuana users appear
healthier and hardier. In others, researchers have found more adverse outcomes in the babies of marijuana users. ...
A study of one-year-olds found no differences between marijuana-exposed and nonexposed babies on measures of health,
temperament, personality, sleeping patterns, eating habits, psychomotor ability, physical development, or mental functioning.
In two studies, one of three-year-olds, the other of four-year-olds, there was no effect of prenatal marijuana exposure
on children’s overall IQ test scores. ...
After controlling for known confounding variables, [Peter A] Fried estimates that prenatal drug exposure accounts for
8 percent or less of the variance in children’s scores on developmental and cognitive tests—and this estimate is for alcohol,
tobacco, and marijuana combined. In essentially all studies, marijuana contributes less than alcohol or tobacco.
In addition, the findings differ from one study to another, and show no consistent relationship of fetal harm to
either the timing or degree of marijuana exposure. While it is sensible to advise women to abstain from all
drugs during pregnancy, the weight of current scientific evidence suggests that marijuana does not directly harm the human fetus."
summarizes Lynn Zimmer, John P Morgan from
"Use of Marijuana During Pregnancy",
Mothering, Feb 22 2010, updated June 20 2013

2002: "Up to approximately 3 years of age there appears to be very little impact upon the
offspring. Beyond that age, in utero cannabis exposure does not impact
upon standardized derived IQ scores but is negatively associated with
attentional behavior and visual analysis/hypothesis testing. These findings
are hypothesized as prenatal marijuana exposure having a negative influence
on aspects of executive function–a “top-down,” multifaceted cognitive
construct involved in organizing and integrating specific cognitive and
output processes over a interval of time. The results and their interpretation
are examined in terms of behavioral teratogenic effects (or lack of effects)
during the various developmental stages of the offspring, the non-unitary
nature of executive function, cannabis receptors, and the consequences of
chronic marijuana use in the non-pregnant population." summarizes Peter A Fried from
"The Consequences of Marijuana Use During Pregnancy: A Review of the Human Literature.",
Journal of Cannabis Therapeutics, vol 2 no 3/4, 2002, pgs 85-104

1998: "Our testing showed that the children of women who used ganja had better alertness, stability and
adjustment than children of women who didn't use ganja. This was measured at the age of one month.
We measured children again at four years and at five years of age, and found that there were no apparent deficits in the
children of marijuana-using mothers. In fact, in many ways, they were better off than children of non-smoking mothers.
The ganja-using mothers also seemed better off than non-users." claims Melanie Dreher
from "Dr. Melanie Dreher, reefer researcher",
Cannabis Culture, Nov 1 1998

Progression

Cannabis use correlation to other drug use and crime
Includes "gateway" theory, "stepping stone" theory, "gatekeeper" theory
Also see Aggression,
Legal Progression

2006: "... National Survey on Drug Use and Health, conducted in 2004,
counted about 97 million Americans who have tried marijuana, compared to
3 million who have tried heroin (166,000 had used
it in the previous month). That's not much of a rush through the gateway.
And a number of studies have demonstrated that your chances of becoming an
addict are higher if addiction runs in your family, or if heroin is readily
available in your community, or if you're a risk-taker. These factors can
account for the total number of heroin addicts, which could make the gateway
theory superfluous. On close inspection, [Mount Sinai School of Medicine
Prof Yasmin] Hurd's research, published in the journal
Neuropsychopharmacology,
doesn't show otherwise. For the most part, it's a blow to the gateway theory.
To be sure, Hurd found that rats who got high on pot as adolescents used
more heroin once they were addicted. But she found no evidence that they
were more likely to become addicted than the rats in the control group who'd
never been exposed to delta-9-tetrahydrocannabinol, or THC, marijuana's main
ingredient. ... The control rats paced their cages and repeatedly pressed
the active bars even when the light indicating availability wasn't on. The
pot rats, on the other hand, figured out that the heroin was available only
at certain times, and that pacing and tapping the bar incessantly wasn't
worth the trouble. When heroin was available, the marijuana rats took more
of it. But when it wasn't, they chilled in the corner." reports Ryan Grim,
"Gateway to Nowhere? The evidence
that pot doesn't lead to heroin.", Slate mag, July 20 2006.

2004: "Another important question about the effects of drug policies
concerns the use of other illicit drugs. The 'separation of markets,' in
which lawfully regulated cannabis distribution reduces the likelyhood that
people seeking cannabis will be drawn into deviant subcultures where 'hard
drugs' also are sold is one public health objective of Dutch decriminalization."
claims claims Craig Reinarman, Peter DA. Cohen, Hendrien L Kaal from
"The
Limited Relevance of Drug Policy: Cannabis in Amsterdam and in San
Francisco", American Journal of Public Health, vol 94, no 5, May
2004, pgs 836-842. Also at
regulatemarijuana.org/pdf/ajph_050104.pdf

2004: "NDTS 2003 data indicate, however, that a relatively small
percentage (4.6%) of state and local law enforcement agencies nationwide
identify marijuana as the drug most contributing to violent crime in their
areas. An association between marijuana and property crime is stronger, as
evidenced by the 11.8 percent of state and local agencies across the country
that identified marijuana as the drug most contributing to property crime
in their areas." claims US
National Drug Intelligence Center from
National
Drug Threat Assessment 2004: Marijuana, Apr 2004.

2003: "In Nevada, more than 67% of teens try marijuana before graduating
from high school. By contrast, in the Netherlands, where marijuana is sold
in indoor establishments to adults who are carded for age, teenage marijuana
use rates are dramatically lower. It would appear that taking marijuana off
the streets and regulating it reduces teen access to marijuana." claims Stop
Teen Use Of Marijuana.
stopteenuse.com/home

2003: "Researchers looked at over 300 pairs of same sex twins, both
identical and non-identical, in which one twin started using cannabis before
his or her 17th birthday and the other did not. ... found that the early
user was two to five times more likely to go on to use harder drugs or become
dependent on alcohol - regardless of whether they
were an identical twin or not. ... not everyone who likes a drink ends up
as a coke addict, but very few users of hard drugs have not tried cannabis
first. The twin study rules out a large genetic component. But it also suggests
that the home and womb environment may not a key factor either, because the
twins shared both and yet early marijuana use in one still raised the chances
of later hard drug use. ... it is impossible to eliminate all nurture differences
between twins. For example, one twin might have suffered a traumatic event
in childhood that did not affect the other. ... The work shows that marijuana
is indeed a gateway to other illicit drugs, says Denise Kandel, at Columbia
University, New York, in an editorial commenting on the journal paper. Therefore,
whatever the appropriate intervention turns out to be, it must be focussed
on young cannabis users, she says." 
"Marijuana's
link to hard drug use not genetic" by James Randerson, New
Scientist, review of Journal of the American Medical Association,
vol 289, pgs 427, 482.

2002: "A new study by the RAND Drug Policy Research Center casts doubt
on claims that marijuana acts as a 'gateway' to the use of
cocaine and heroin, challenging
an assumption that has guided US drug policies since the 1950s. ... 'We've
shown that the marijuana gateway effect is not the best explanation for the
link between marijuana use and the use of harder drugs,' said Andrew Morral,
associate director of RAND's Public Safety and Justice unit and lead author
of the study. 'An alternative, simpler and more compelling explanation accounts
for the pattern of drug use you see in this country, without resort to any
gateway effects. While the gateway theory has enjoyed popular acceptance,
scientists have always had their doubts. Our study shows that these doubts
are justified.' The study demonstrates that associations between marijuana
and hard drug use could be expected even if marijuana use has no gateway
effect. Instead, the associations can result from known differences in the
ages at which youths have opportunities to use marijuana and hard drugs,
and known variations in individuals' willingness to try any drugs, researchers
found. ... 'The people who are predisposed to use drugs and have the opportunity
to use drugs are more likely than others to use both marijuana and harder
drugs," Morral said. "Marijuana typically comes first because it is more
available. Once we incorporated these facts into our mathematical model of
adolescent drug use, we could explain all of the drug use associations that
have been cited as evidence of marijuana's gateway effect.' ... RAND researchers
tested the marijuana gateway theory by creating a mathematical model simulating
adolescent drug use. Rates of marijuana and hard drug use in the model matched
those observed in survey data collected from representative samples of youths
from across the United States. Without assuming any gateway effect, the model
produced patterns of drug use and abuse remarkably similar to what is experienced
across the nation, showing that a marijuana gateway effect is not needed
to explain the observed behavior." claims RAND Drug Policy Research Center
from
"RAND
Study Casts Doubt on Claims That Marijuana Acts as 'Gateway' to the Use of
Cocaine and Heroin", Dec 2 2002.

1999: "There is no conclusive evidence that the drug effects of marijuana
are causally linked to the subsequent abuse of other illicit drugs. ... Patterns
in progression of drug use from adolescence to adulthood are strikingly regular.
Because it is the most widely used illicit drug, marijuana is predictably
the first illicit drug most people encounter. Not surprisingly, most users
of other illicit drugs have used marijuana first. In fact, most drug users
begin with alcohol and nicotine
before marijuana, usually before they are of legal age." claims Janet E Joy,
Stanley J Watson Jr, and John A Benson Jr,
Marijuana
and Medicine: Assessing the Science Base, Division of Neuroscience
and Behavioral Research, Institute of Medicine (Washington, DC: National
Academy Press, 1999).

1997: "Long-term studies consistently show that only one in five youthful
pot smokers will ever try harder drugs such as cocaineheroin, or
methamphetamine, and fewer than one in 25
will use hard drugs regularly. The upshot is not that marijuana leads the
masses to hard stuff, but that the few who use stronger drugs will not say
no to weaker ones. (For the latest summary of research demolishing "reefer
madness 1997," see Rolling Stone, 2/20/97.)" claims Mike Males from
"Why Are
Media Enlisting in the Government's Crusade Against Marijuana?", July/Aug
1997.

1994: "Children who use marijuana are 85 times more likely to use
cocaine than non-marijuana users. (Ninety percent
of children who used marijuana smoked or drank first.) ... Adults who used
marijuana as children are 17 times more likely to be regular
cocaine users. (Ninety-one percent of adults who used
marijuana as children smoked or drank first.)" claims
Joseph A Califano, Jr, Center
on Addiction and Substance Abuse (CASA) at Columbia, Oct 27, 1994.

1995: "The primary basis for this 'gateway hypothesis' is a recent
report by the Center on Addiction and Substance Abuse (CASA), claiming that
marijuana users are 85 times more likely than non-marijuana users to try
cocaine. This figure, using data from NIDA's 1991
National Household Survey on Drug Abuse, is close to being meaningless. It
was calculated by dividing the proportion of marijuana users who have ever
used cocaine (17%) by the proportion of cocaine users who have never used
marijuana (.2%). The high risk-factor obtained is a product not of the fact
that so many marijuana users use cocaine but that so many cocaine users used
marijuana previously. It is hardly a revelation that people who use one of
the least popular drugs are likely to use the more popular ones  not
only marijuana, but also alcohol and
tobacco cigarettes. The obvious statistic not publicized
by CASA is that most marijuana users  83 percent  never use cocaine.
Indeed, for the nearly 70 million Americans who have tried marijuana, it
is clearly a 'terminus' rather than a 'gateway' drug." claim
John P Morgan and
Lynn Zimmer (deceased)
in "The
Myth of Marijuana's Gateway Effect", Feb 7 1995.

1972: "Rather than inducing violent or aggressive behavior through
its purported effects of lowering inhibitions, weakening impulse control
and heightening aggressive tendencies, marihuana was usually found to inhibit
the expression of aggressive impulses by pacifying the user, interfering
with muscular coordination, reducing psychomotor activities and generally
producing states of drowsiness lethargy, timidity and passivity." claims
Raymond P Shafer, et al,
Marihuana: A Signal of Misunderstanding, National Commission on Marihuana
and Drug Abuse.

1968: "It can clearly be argued on the world picture that cannabis
use does not lead to heroin addiction." claims British
Advisory Committee on Drug Dependence in The Wooten Report: Committee
on Drug Dependence, Cannabis

Reproductive System

2009: "Frequent and/or long-term marijuana use may significantly increase
a man's risk of developing the most aggressive type of testicular
cancer, according to a study by researchers at
Fred Hutchinson Cancer Research Center. The study results were published
online Feb 9 in the journal Cancer. The researchers found that being
a marijuana smoker at the time of diagnosis was associated with a 70 percent
increased risk of testicular cancer. The risk was particularly elevated (about
twice that of those who never smoked marijuana) for those who used marijuana
at least weekly and/or who had long-term exposure to the substance beginning
in adolescence. The results also suggested that the association with marijuana
use might be limited to nonseminoma, a fast-growing testicular malignancy
that tends to strike early, between ages 20 and 35, and accounts for about
40 percent of all testicular-cancer cases. ... The researchers emphasize
that their results are not definitive, but rather open a door to more research
questions. 'Our study is the first inkling that marijuana use may be associated
with testicular cancer, and we still have a lot of unanswered questions,'
[Stephen M] Schwartz said, such as why marijuana appears to be associated
with only one type of testicular cancer. 'We need to conduct additional research
to see whether the association can be observed in other populations' ...
The National Cancer Institute, the National Institute on Drug Abuse and funds
from the Hutchinson Center supported this research ... According to the National
Cancer Institute, testicular cancer is very rare, accounting for only 1 percent
of cancers in U.S. men. About 8,000 men are diagnosed with testicular cancer
each year, and about 390 die of the disease annually." 
"Marijuana
Use Linked to Increased Risk of Testicular Cancer", Feb 9 2009. Related
articles:
"Association
of Marijuana Use and the Incidence of Testicular Germ Cell Tumors",
"Marijuana
Linked to Aggressive Testicular Cancer"

2003: "Men who smoke marijuana frequently have significantly less
seminal fluid, a lower total sperm count and their sperm behave abnormally,
all of which may affect fertility adversely, a new study in reproductive
physiology at the University at Buffalo has shown. This study is the first
to assess marijuana's effects on specific swimming behavior of sperm from
marijuana smokers and to compare the results with sperm from men with confirmed
fertility. Marijuana contains the cannabinoid drug THC (tetrahydrocannabinol),
which is its primary psychoactive chemical, as well as other cannabinoids."
claims Lani J Burkman from
"Sperm
From Marijuana Smokers Move Too Fast Too Early, Impairing Fertility, UB Research
Shows", Oct 14 2003

1991: "Chronic use of marijuana didn't affect concentrations of any
of these hormones [testosterone, lutenizing hormone, follicle stimulating
hormone, prolactin, and cortisol] The finding of decreased testosterone levels
in men continues today to be widely disseminated in the informational literature
even though subsequent research hasn't supported the 1974 findings." claims
Dr Robert Block, Assistant Professor of Anesthesia, Iowa College of Medicine
and author of an article published in the journal Drug and Alcohol
Dependence.

1978: "Federally funded studies of long-tern users of high-potency
marijuana in three foreign countries showed no difference between the health,
ability to work, and brain function of users and non-users, a number of
researchers said ... The studies failed, however, to settle a recent controversy
over whether marijuana smoking reduces the amount of the male sex hormone
testosterone, as originally reported by Dr Robert C Kolodny of the Reproductive
Biology Research Foundation in St Louis. A comparison of 84 Costa Rican marijuana
users with 156 nonusers by a team of doctors headed by W J Coggins of the
University of Florida turned up no difference in testosterone levels. But
[Dr Sidney] Cohen's studies at UCLA backed Kolodny's findings. ... In studying
the health of American users, Cohen kept 28 men who used marijuana in the
UCLA hospital and studied their reactions. He found the lowered testosterone
levels ..." reports Stuart Auerbach in "Studies See No Health Effect of Pot
Smoking, Researchers Say", Washington Post, Jan 28, 1978.

"Although initial use of cannabis lowers sperm count and testosterone levels,
animals and humans develop a tolerance after prolonged use, with sperm count
and testosterone returning to levels found in non-users." claims a study,
Cannnabis in Costa Rica: A Study of Chronic Marijuana Use, by William
Carter.

Smoking

2005: "Marijuana smoking -'even heavy longterm use'- does not cause
cancer of the lung, upper airwaves, or esophagus,
Donald Tashkin reported at this
year's meeting of the International Cannabinoid Research Society. Coming
from Tashkin, this conclusion had extra significance for the assembled
drug-company and university-based scientists (most of whom get funding from
the U.S. National Institute on Drug Abuse). Over the years, Tashkin's lab
at UCLA has produced irrefutable evidence of the damage that marijuana smoke
wreaks on bronchial tissue. With NIDA's support, Tashkin and colleagues have
identified the potent carcinogens in marijuana smoke, biopsied and made
photomicrographs of pre-malignant cells, and studied the molecular changes
occurring within them. It is Tashkin's research that the Drug Czar's office
cites in ads linking marijuana to lung cancer. Tashkin himself has long believed
in a causal relationship, despite a study in which Stephen Sidney examined
the files of 64,000 Kaiser patients and found that marijuana users didn't
develop lung cancer at a higher rate or die earlier than non-users. Of five
smaller studies on the question, only two -involving a total of about 300
patients- concluded that marijuana smoking causes lung cancer. Tashkin decided
to settle the question by conducting a large, prospectively designed,
population-based, case-controlled study. 'Our major hypothesis,' he told
the ICRS, 'was that heavy, longterm use of marijuana will increase the risk
of lung and upper-airwaves cancers.' ... Exposure to marijuana was measured
in joint years (joints per day x 365). Controls were found based on age,
gender and neighborhood. Among them, 46% had never used marijuana, 31% had
used less than one joint year, 12% had used 10-30 j-yrs, 2% had used 30-60
j-yrs, and 3% had used for more than 60 j-yrs. Tashkin controlled for
tobacco use and calculated the relative risk of marijuana
use resulting in lung and upper airwaves cancers. All the odds ratios turned
out to be less than one (one being equal to the control group's chances)!
Compared with subjects who had used less than one joint year, the estimated
odds ratios for lung cancer were .78; for 1-10 j-yrs, .74; for 10-30 j-yrs,
.85 for 30-60 j-yrs; and 0.81 for more than 60 j-yrs. The estimated odds
ratios for oral/pharyngeal cancers were 0.92 for 1-10 j-yrs; 0.89 for 10-30
j-yrs; 0.81 for 30-60 j-yrs; and 1.0 for more than 60 j-yrs. ... 'So, in
summary' Tashkin concluded, 'we failed to observe a positive association
of marijuana use and other potential confounders.' " reports
Fred Gardner from
"Study:
Smoking Marijuana Does Not Cause Lung Cancer", CounterPunch, July
2-4 2005.

2004: "Previous laboratory investigations, case reports, and a
hospital-based case-control study have suggested that marijuana use may be
a risk factor for squamous cell head and neck cancer. We conducted a
population-based case-control study to determine whether marijuana use is
associated with the development of oral squamous cell carcinoma (OSCC). Case
subjects (n = 407) were 1865-year-old residents of three counties in
western Washington State who were newly diagnosed with OSCC from 1985 through
1995. Control subjects (n = 615), who were similar to the cases with respect
to age and sex, were selected from the general population using random-digit
telephone dialing. Lifetime histories of marijuana use and exposure to known
OSCC risk factors were ascertained using a structured questionnaire. Information
on genetic polymorphisms in glutathione S-transferase enzymes was obtained
from assays on participant DNA. Odds ratios for associations with features
of marijuana use were adjusted for sex, education, birth year,
alcohol consumption, and
cigarette smoking. A similar proportion of case subjects
(25.6%) and control subjects (24.4%) reported ever use of marijuana (adjusted
odds ratio, 0.9; 95% confidence interval, 0.61.3). There were no trends
in risk observed with increasing duration or average frequency of use or
time since first or last use. No subgroup defined by known or suspected OSCC
risk factors (age, cigarette smoking, alcohol consumption, and genetic
polymorphisms) showed an increased risk. Marijuana use was not associated
with OSCC risk in this large, population-based study." claims Karin A.
Rosenblatt1, Janet R. Daling2,3, Chu Chen2,3, Karen J. Sherman4 and Stephen
M. Schwartz, from
"Marijuana
Use and Risk of Oral Squamous Cell Carcinoma", Cancer Research #64,
June 1 2004, pgs 4049-4054.

2003: "Although the inhalation of chemical toxins in cannabis smoke
has been linked to bronchitis and other respiratory problems, it has not
been shown to cause lung cancer or a higher death rate. The most extensive
study to date on marijuana and mortality was conducted by investigators at
Kaiser Permanente and published in the April 1997 issue of the American
Journal of Public Health. It showed no substantial link between regular
marijuana smoking and death, but suggested that marijuana prohibition may
itself pose a health hazard to the user. The Kaiser team, led by Stephen
Sidney, MD, looked at 10 years of mortality statistics for more than 65,000
men and women who received health check-ups at Kaisers Oakland and
San Francisco hospitals between 1979 and 1985. Patients were divided into
groups ranging from those who had never tried marijuana to those who use
it currently or regularly. Mortality statistics for all patients were followed
until 1991 and analyzed for any association between marijuana and death.
The studys statistical methodology controlled for the use of
tobacco and alcohol so that
deaths from marijuana smoking could be clearly defined. Researchers found
no increase in deaths among the more than 14,000 patients who reported they
were marijuana users as compared to those who had never used marijuana. They
further noted that the total mortality risks associated with marijuana use
were lower than those for tobacco-cigarette smoking for both men and women.
Women who used marijuana also had a lower risk of total mortality as compared
to those who consumed alcohol regularly. The study
noted that marijuana smokers with AIDS did have a significantly higher death
rate than non-smokers, but said that their mortality was virtually the same
as it was for AIDS patients who didnt smoke marijuana. Researchers
stressed that the links they found between marijuana use and death were
associations and not an indication that marijuana was a cause of death.
from
"Marijuana
Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Jouurnal
of the California Cannabis Research Medical Group, Summer 2003.

1999: "Recent reports of molecular and genetic alterations in marijuana
users suggested that marijuana smoke might also activate CYP1A1 gene. Dr.
Roth investigated this possibility using Hepa-1 cells and found that marijuana
tar, and more specifically D9-THC, regulates the induction and function of
CYP1A1 gene, an observation that is entirely novel. Transcriptional activation
of CYP1A1 by D9-THC may help to explain the relatively high frequency of
DNA mutations and mucosal abnormalities that occur in marijuana smokers.
The inhalation of marijuana smoke delivers both nanogram concentrations of
conventional PAHs and milligram quantities of D9-THC to the lung. Induction
of CYP1A1 produced by D9-THC could result in greater activation of smoke-related
procarcinogens and higher adduct-related injury. However, it is also possible
that inhaled D9-THC competes for the active site of CYP1A1, paradoxically
reducing the activation of procarcinogens." claims Dr Michael D Roth from
"A
Conference Summary on Pulmonary Pathophysiologic and Immune Consequences
of Smoked Substance Abuse", National Institute on Drug Abuse.

1995: "The smoking of cannabis, even long term, is not harmful to
health." claims the British scientific journal Lancet.

1993: "This water pipe study is a classic example of the harm reduction
approach to drug use. If water pipes really reduce the harm associated with
marijuana smoking, non-medical users can be educated about the benefits of
water pipes and encouraged to use them whenever possible. Since smoking is
one of the main harms associated with the use of marijuana (accidents are
another), this simple water pipe study may help lay the groundwork for
significantly reducing the harmfulness of marijuana smoke. If US drug policy
ever moves to a harm-reduction approach to marijuana, studies such as this
one will play an important role in helping users to identify and minimize
the health risks of marijuana." claims Gieringer,
"Marijuana
Water Pipe Study", Newsletter of the Multidisciplinary Association
for Psychedelic Studies, Vol 4, No 3, Winter 1993-94.

2004: "I'm fighting for the right to use cannabis to prevent
uncontrollable seizures where over 20 Rx meds and surgery have failed....
My mother has had epilepsy all her life. Most of her life she was able to
control her seizures with dilantin, Phenobarbital and most recently Tegretol.
About 5 years ago she started having auras and seizures that no prescription
medication was able to control. ... The reason I'm writing is because we
know that cannabis (marijuana) prevents her seizures. Not only do I know
this but there are thousands of other patients out there that know it. ...
The Ohio State Medical Society convened a committee that reported on the
medicinal properties of cannabis in 1860. W.P. Kincaid reported: I
have treated four cases of epilepsy with the hemp; two were permanently benefited
(at least to the present time); one temporarily, and one not at all.
Major pharmaceutical firms listed epilepsy as one of the conditions for which
cannabis was indicated either alone or as an ingredient in combination
preparations." claims "phatboy" 
"5000
year old drug prevents seizures.", Epilepsy Foundation eCommunities Forums,
Jan 8 2004.

2003: "The majority of respondents (96%) was aware cannabis was
potentially therapeutically useful for MS and most (72%) supported legalization
for medicinal purposes. ... Symptoms reported to be ameliorated included
anxiety/depression, spasticity and chronic pain. ... Conclusions: Subjective
improvements in symptom experience were reported by the majority of people
with MS who currently use cannabis. Further evaluation of this substance
is warranted." claims Page SA, Verhoef MJ, Stebbins RA, Metz LM, Levy JC,
"Cannabis use as described by people with multiple sclerosis.",
Canadian Journal
of Neurological Sciences, Aug 2003, pgs 201-205.

2002: "There is a growing amount of evidence to suggest that cannabis
and individual cannabinoids may be effective in suppressing certain symptoms
of multiple sclerosis and spinal cord injury, including spasticity and pain.
... Clinical trials have shown that cannabis, Delta(9)-tetrahydrocannabinol,
and nabilone can produce objective and/or subjective relief from spasticity,
pain, tremor, and nocturia in patients with multiple sclerosis (8 trials)
or spinal cord injury (1 trial). The clinical evidence is supported by results
from experiments with animal models of multiple scleroisis." claims Pertwee
RG, "Cannabinoids and multiple sclerosis.", Pharmacological
Therapeutics, Aug 2002, pgs 165-174.

2000: "I've heard that Dilantin is ~ the World's best anti-seizure
drug and that it can be a very effective, fast-acting anti-depressant. Also,
as I recall, one animal study was done with Dilantin and it ~ significantly
extended the average lifespan of the animals. ... the full suite of Cannabinoids
from the Cannabis Plant perform together as the World's most effective
anti-seizure 'agent' or combination. Also, this herbal extract blend of
Cannabinoids is a very safe and effective anti-depressant medicine ..." claims
Pat from "Cannabis
vs Dilantin. Safety Ratio. WoDs, etc.", Marihemp, July 2
2000.2003: "Treatment with [Marinol] cannabinoids did not have a
beneficial effect on spasticity when assessed with the Ashworth scale. However,
though there was a degree of unmasking among the patients in the active treatment
groups, objective improvement in mobility and patients' opinion of an improvement
in pain suggest [Marinol] cannabinoids might be clinically useful." claims
John Zajicek, Patrick Fox, Hilary Sanders, David Wright, Jane Vickery, Andrew
Nunn, Alan Thompson, "Cannabinoids for treatment of spasticity and other
symptoms related to multiple sclerosis (CAMS study): multicentre randomised
placebo-controlled trial",
The Lancet,
vol 362, no 9395, Nov 2003.thelancet.com/journal/vol362/iss9395/full/llan.362.9395.original_research.27670.1

2000: "The exacerbation of these signs after antagonism of the CB1
and CB2 receptors, notably the CB1 receptor, using SR141716A and SR144528
(ref 8) indicated that the endogenous cannabinoid system may be tonically
active in the control of tremor and spasticity. This provides a rationale
for patients' indications of the therapeutic potential of cannabis in the
control of the symptoms of multiple sclerosis ..." claims Baker D, Pryce
G, Croxford JL, Brown P, Pertwee RG, Huffman JW, Layward L, "Cannabinoids
control spasticity and tremor in a multiple sclerosis model.", Nature,
Mar 2000, pgs 84-87.

1989: "The chronic motor handicaps of a 30-year-old multiple sclerosis
patient acutely improved while he smoked a marihuana cigarette. ... It is
concluded that cannabinoids may have powerful beneficial effects on both
spasticity and ataxia that warrant further evaluation." claims Meinck HM,
Schonle PW, Conrad B, "Effect of cannabinoids on spasticity and ataxia in
multiple sclerosis.", Journal of Neurology, Feb 1989, pgs 120-122.

1987: "At doses greater than 7.5 mg [of THC] there was significant
improvement in patient ratings of spasticity compared to placebo. These positive
findings in a treatment failure population suggest a role for THC in the
treatment of spasticity in multiple sclerosis." claims Ungerleider JT, Andyrsiak
T, Fairbanks L, Ellison GW, Myers LW, "Delta-9-THC in the tratment of spasticity
associated with multiple sclerosis.", Adv Alcohol Substance Abuse,
1987, pgs 39-50.

1981: "For the group, 10 mg THC significantly reduced spasticity by
clinical measurement (P less than 0.01). Quadiceps EMG interference pattern
was reduced in those four patients with primarily extensor spasticity. THC
was administred to eight other patients with spasticity and other CNS lesions.
Responses varied, but benefit was seen in three of three patients with 'tonic
spasms.' " claims Petro DJ, Ellenberger C Jr, "Treatment of human spasticity
with delta 9-tetrahydorcannabinol.", Journal of Clinical Pharmacology,
Aug-Sept 1981, pgs 413S-416S.

"In 1839, Dr. William B. O'Shaughnessy was greatly impressed with the plant's
muscle relaxant and anti-convulsant properties, stating his belief that in
cannabis, 'The (medical) profession has gained an anti-convulsive remedy
of the greatest value.' An historical account alluding to the use of cannabis
in the treatment of spasticity can be found in a March 22, 1890, issue of
The Lancet. An article written by Dr. J. Russell Reynolds (physician
to Queen Victoria) noted, 'There are many cases of so called epilepsy in
adults but which, in my opinion (are) the result of organic disease of a
gross character in the nervous centers, in which India hemp (cannabis) is
the most useful agent with which I am acquainted.' Dr. Reynolds may well
have been referring to multiple sclerosis (MS). The first written record
of MS is noted between 1880-85. ... Muscular spasticity ... afflicts individuals
with multiple sclerosis, stroke, cerebral palsy, paraplegia, quadriplegia,
and spinal cord injuries. Current medical therapy is woefully inadequate
for those individuals suffering from spasticity problems. ... a significant
number of studies have been conducted leading Chief Administrative Law Judge
Francis Young of the DEA to conclude
in September 1988 that marijuana's medical benefits in the treatment of
spasticity is 'beyond question' and recommended rescheduling of the drug
to allow prescriptive access. Unfortunately Judge Young's ruling was rejected
by the administrator of the DEA." claims Alliance for Cannabis Thearpeutics
from
"Medical
Use of Marijuana for Muscular Spasticity".

"Cannabinoids act in general as inhibitory neurotransmitters, meaning that
they inhibit processes that other neurotransmitters can stimulate. This is
probably why cannabinoids are such effective anti-spasmodic agents. Cannabinoid
receptors are very rich in the areas of the brain that control muscle spasms."
claims Los Angeles Cannabis Resource Center from
"Cannabinoids in
the Brain".

"I encountered spasticity as a major stumbling block to rehab. They attempted
to control the spasms with Valium for 3 months and my mind was so fogged
that I revolted and asked to be removed from Valium  I couldn't remember
anything. I then was prescribed Leorisal whose generic name is Baclofen 
200 mg every 4 hours for the last 27 years. It  along with range of
motion exercise  allays the spasms to a manageable extent. My legs
shake uncontrollably  they violently jump, stick out straight in front
and don't bend at the knee. Baclofen is supposed to control this but it doesn't.
Episodes of spasms during the time of my rehab were violent and embarrassing.
Two Vietnam vets who were in rehab with me took mercy on me. One night, they
took me to the roof for 'fresh air' where we smoked a marijuana joint, which
immediately not only affected my mood but also affected the spasms. ... A
joint the morning and two or three in the evening keep me upbeat and spasm
free, coupled with range of motion exercise and a healthy diet. I don't want
to take Valuim or other incapacitating drugs even though I could. The marijuana
allows me to keep an even keel and to avoid episodes of spasms. If I took
Baclofin alone, I would not have this level of control. I would still have
spasms." claims anonymous spinal injuried paraplegic from Arkansas, from
"Patient
Story - Spinal Injury".

"The nerves in my neck were smashed in a gunshot accident ... I can move
my arm, but I can't move my fingers. There is a kind of numbness from my
left shoulder down to my pinkie. But there is also a burning feeling, like
needles. I can't stand for anything to touch my arm  if I accidently
hit it there is extreme pain. It throbs 24 hrs a day. I've been on numerous
strong medicines, including Tawan NX, Vicodin 10 mg
[hydrocodone and
acetaminophen] , and
methadone 10 mg 4 to 5 pills per day. Some days I
can take less, depending on how much I use marijuana. I don't smoke to get
stoned, I smoke it for relief from thinking about my arm all the time and
to take away the pain. When I smoke marijuana, I can get things done around
the house, it gets me energetic, gives me an appetite. I don't have an appetite
when I don't have marijuana  I have to force myself to eat. The narcotics
give you a state of mind where you don't eat  I had to get off Vicodin
 I was taking too much  it was hurting my kidneys. There's some
kind of aspirin in it, 600 mg per tablet, 5-6 tablets per day  we caught
it just in time before it ruined my kidneys. So they put me back on methadone
 I didn't want to get back on that  it makes me nauseated, not
eat, sometimes makes me depressed. When I smoke, I don't have to take very
much methadone and I have a better outlook on life." claims anonymous patient
from
"Nerve
Damage".

Stress

1999: On Aug 6, B E Smith, the first Californian to fight federal
drug charges using the state's voter-approved medical marijuana law was sentenced
to 27 months in prison. Proposition 215 could have shielded Smith in state
court because he has a doctor's recommendation to grow and smoke the plant
to relieve post-traumatic stress disorder from his service in Vietnam.

Temporo-Mandibular Joint Disorder (TMJ)

"I have hypoglycemia, a form of diabetes. ... The second condition I treat
with marijuana is TMJ disorder, referring to the temporo-mandibular joint
of the jaw. Over the years, this condition has worn my cartilage away. The
severity of pain is hard to describe, but if the pain was ranked in levels
up to 5, I would say that level 3 I am nauseated from the pain. At level
4 I can barely move my jaws enough to talk and eating is difficult. The real
challenge is to not vomit from the pain, because vomiting flexes my jaw.
At level 5, I can't avoid vomiting and I can't eat, which causes my blood
sugar to drop dangerously low. The standard treatments for this are cortisone
shots in the jaw and/or joint replacement. I have a history of drug allergies
and am afraid to use cortisone. Also, I've learned that jaw joint replacement
is very risky with low success rates. ... I wear a bite plate to keep my
teeth apart while I sleep. I have a TENS machine that I wear that sends
electro-shock to my jaws, which helps bring the pain down a little but I
can only use it for one and half hours at a time. For the pain, I've tried
Vicodin [hydrocodone and
acetaminophen] , but marijuana is as effective
as two Vicodin and the relief is immediate with easily controlled dosage.
For the nausea and vomiting, marijuana is amazing. The nausea stops in two
minutes, period. Even if I'm already vomiting, I can still get it in my system
with a few puffs. Since I was arrested, I have struggled because they threaten
me with drug tests and jail. I've experimented with more chemical medications.
The first month after my arrest I lost twenty pounds, and I was already
underweight. The doctor was trying me on different drugs and my body was
not tolerating them, so he switched me from one to another six or eight times.
I was desperate, but I didn't want to take narcotics. I've been on Vicodin
since December 2001, which is a very addicting drug and not recommended for
long term use. Not only am I having symptoms of physical addiction, but it's
making my condition worse by staying in my system too long and putting me
into deep sleep which causes my blood sugar to drop. So the episodes that
normally last 4-5 days are now lasting two weeks or more. When it finally
eases up, I go through withdrawal. ... I believe God put marijuana on Earth
as medicine to help people. I don't believe opiate addiction is part of God's
plan for me. I could leave my home and family for a state where medical marijuana
laws would protect me, but I am a grandmother and a granddaughter and don't
want to leave my loved ones. ... Our doctor would recommend marijuana if
he didn't face the threat of losing his license." claims anonymous female
patient from
"Appetite
and Pain".

Tetra-Hydro-Cannabinol (THC)

2010: "A combination of compounds in marijuana could help fight off
a particularly deadly form of braincancer, preliminary research suggests. Researchers
at the California Pacific Medical Center Research Institute (CPMCRI) combined
the non-psychoactive Cannabis compound,
cannabidiol (CBD), with 9-tetrahyrdocannabinol
(9-THC), the primary psychoactive active ingredient in Cannabis. They found
the combination boosts the inhibitory effects of 9-THC on glioblastoma, the
most common and aggressive form of brain tumor. 'Our study not only suggests
that combining these two compounds creates a synergistic effect but it also
helps identify molecular mechanisms at work here, and that may lead to more
effective treatments for glioblastoma and potentially other aggressive cancers',
said Sean McAllister, a scientist at CPMCRI and the lead author of the study."

"Marijuana
compounds may help fight brain cancer", Jan 16 2010

2005: "There are sound medical reasons for spraying cannabis under
the tongue rather than smoking or eating it. The mucosa of the mouth will
absorb the drug faster than the digestive system, indeed almost as fast as
the lungs, but without irritating the respiratory system. And Sativex can
be precisely metered  a single one-tenth milliliter spray contains
2.7 milligrams of tetrahydrocannabinol (THC), pot's main psychoactive chemical;
2.5 milligrams of cannabidiol, which doctors think reduces anxiety and muscle
tension; and all of pot's active ingredients known as cannabinoids 
so that it can be accurately studied." reports Gary Greenberg,
"Respectable Reefer",
Nov 14 2005

2005: "Health Canada's approval of Sativex was based on the results
of a four-week clinical trial involving 66 patients with MS-related neuropathic
pain that was carried out in Great Britain, in which half received Sativex
and the other half received a placebo. ... Sativex isolates the cannabinoid
components, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD),
representing only two of the more than 60 related chemicals that make up
the marijuana plant. It is believed that THC helps patients with pain while
CBD has a neurological effect, and that isolating these two cannabinoids
will enable patients to eliminate many of the side-effects that are associated
with the use of medical marijuana." reports David Hodges,
"Pot-based
drug shows promise for neuropathic pain", Medical Post vol 41
issue 19, May 17 2005.

2004: "Cannabis extracts may be well suited to treatment of inflammatory
diesases due to their multiple mechanisms of action. THC seemingly alleviates
pain, spasm and diarrhoea, while the CBD component presents the likelyhood
of immunomodulatory benefits. One recently demonstrated CBD effect is its
ability to inhibit TFN-a (tissue necrosis factor-alpha), a proven mechanism
of other agents employed to treat inflammatory bowel disease." reports
"Which
Conditions Are Treatable With Cannabis?", O'Shaughnessy's Journal
of the California Cannabis Research Medical Group, Spring 2004, citing
"The nonpsychoactive cannabis constiuent cannabidiol is an oral anti-artritic
therapeutic in murine collagen-induced arthritis." by AM Mafait, R Gallily,
PF Sumariwalla, AS Malik, E Andreakos, R Mechoulam, et al, Proceedings
of National Academy of Sciences USA 2000;97(17), pgs 9561-9566.

2003: "Treatment with [Marinol] cannabinoids did not have a beneficial
effect on spasticity when assessed with the Ashworth scale. However, though
there was a degree of unmasking among the patients in the active treatment
groups, objective improvement in mobility and patients' opinion of an improvement
in pain suggest [Marinol] cannabinoids might be clinically useful." claims
John Zajicek, Patrick Fox, Hilary Sanders, David Wright, Jane Vickery, Andrew
Nunn, Alan Thompson, "Cannabinoids for treatment of spasticity and other
symptoms related to multiple sclerosis (CAMS study): multicentre randomised
placebo-controlled trial",
The Lancet,
vol 362, no 9395, Nov 2003.thelancet.com/journal/vol362/iss9395/full/llan.362.9395.original_research.27670.1

2000: "A study by researchers from the University of California, San
Francisco has found that patients with HIV infection taking protease inhibitors
do not experience short-term adverse virologic effects from using cannabinoids.
... All three groups gained weight. Part of that was due to regularly scheduled
meals and snacks being readily available. However, the placebo arm averaged
a gain of 1.30 kilograms while the subjects who took oral dronabinol gained
an average of 3.18 kilograms. Those who smoked marijuana gained an average
of 3.51 kilograms. Caloric intake reflected the same order." claims Dr
Donald I Abrams, Professor of Clinical
Medicine, University of California at San Francisco from
"Marijuana
Does Not Appear To Alter Viral Loads of HIV Patients Taking Protease
Inhibitors", July 13 2000.
also at
cannabismd.org/reports/abrams1.php,
marijuananews.com/news.php3?sid=253

1997: "Synthetic tetrahydrocannabinol, the primary psychoactive ingredient
in marijuana, is currently available in oral form for treatment of HIV Wasting
Syndrome and chemotherapy-induced nausea. A double-blind study confirmed
that this synthetic drug was preferred by chemotherapy patients by an almost
two-to one margin." claims "Marijuana: Myths and Truth", Office of National
Drug Control Policy

1996: "William Anderson is a 37 year old patient of mine who suffers
from severe post traumatic headaches. ... Presently he is taking Tylox
[oxycodone and
acetaminophen] 1 or 2 per day for severe
headaches, Marinol to provide some daily control and Doxipin
[dibenzoxepin] and Lithium to control the depression associated with
his constant turmoil. ... The only drug that seems to give William any
true felief from pain is that from smoking marijuana. ... Having seen him
in constant pain without the availability of the Marinol or marijuana purchased
from a street dealer, I have no question that there is pain relief afforded
to him by the drug. It should be noted that the Marinol only gives him partial
and inadequate pain relief." claims Dr Michael E Mayle, DO, in a letter to
Whom It May Concern, 1996.

1996: 80% of AIDS patients who had used cannabis preferred it to
prescription drugs including synthetic THC, claims B Wesner, "The Medical
Marijuana Issue Among PWAs: Reports of Therapeutic Use and Attitudes Toward
Legal Reform", Drug Research Unit, Social Science Research Institute, University
of Hawaii at Manoa.

1988: "Marijuana cigarettes in many cses are superior to synthetic
THC capsules in
reducing ;chemotherapy-induced
nausea and vomiting. Marijuana cigarettes have an
important, clear advantage over synthetic THC capsules in that natural marijuana
is inhaled and generally takes effect more quickly than the synthetic capsule"
claims Francis L Young, Chief
Administrative Law Judge, US Drug Enforcement Administration, 1988.

1986: "I started feeling the changes pretty much right away. Smoking
marijuana also felt ten times better than taking Marinol pill. It helped
reduce my nausea and I could hold down food better."
claims Jim Kerns, cancer and
chemotherapy patient.

1983: Inhaled botanical cannabis is "far superior to the best available
conventional drug, Compazine, and clearly superior to synthetic THC pill."
claims the report of The Lynn Pierson Therapeutic Research Program, Behavioral
Health Sciences Div, Health and Environment Department, State of New Mexico.

1983: "We found both marijuana smoking and THC capsules to be effective
antiemetics. We found an approximate 23 percent higher success rate among
those patients smoking (90%) than among those administered THC capsules (67%).
... We found that the major reason for smoking failure was smoking intolerance;
while the major reason for THC capsule failure was nausea and vomiting so
severe that the patient could not retain the capsule." claims "Annual Report:
Evaluation of Marijuana and Tetrahydrocannabinol in the Treatment of Nausea
and/or Vomiting Associated with Cancer Therapy Unresponsive to Conventional
Anti-Emetic Therapy: Efficacy and Toxicity", Board of Pharmacy, State of
Tennessee, July 1983.

"When our daughter was undergoing chemotherapy for lymph cancer, she was
sick and vomiting constantly as a result of her treatments. No legal drugs,
including Marinol, helped her. We finally turned to marijuana. With it, she
kept her food down, was comfortable and even gained weight. Those who say
Marinol and other drugs are satisfactory substitutes for marijuana may be
right in some cases but certainly not in all cases." claims
Franklyn "Lyn" Nofziger from
his op-ed published in Washington Post, requoted in
"Medical
Marijuana: Reagan Aide Lyn Nofziger Dead at 81  Supported Patients'
Rights".

Tolerance

Tourette's Syndrome

"I have had Tourette's syndrome almost all of my life. ... In the fifth grade
I started taking Tranxene (clorazepate) 7.5 mg to 'control' my tics. I turned
into a different person. I didn't care about nothing. Then I got on such
a dosage that I didn't do anything but sit and sleep. And I always felt angry,
but yet embarrassed. In about seventh grade the Tranxene started to not work
as well. I started mimicking the teachers, tapping my pencils harder to the
point of breaking them, blinking my eyes really bad, rolling my lips, shaking
my head, and constantly getting up and down out of the chairs. ... Dr. H
... diagnosed me with a full-blown case of Tourette's syndrome and put me
on clonidine 0.1 mg. I had to build myself into it until I was taking three
full pills a day. At that point my life was not mine. I couldn't remember
anything. I didn't do anything. I flunked everything in school, got kicked
out for sleeping in class. 1 was so sad and full of confusion and hate. Then
the clonidine wasn't working so well so I started taking Haldol (haloperidol)
0.5 mg along with the clonidine. I was a zombie by then. I didn't function.
... Paul one night ... asked if I wanted to get high. ... I remember that
first time I was so mellow and actually got pretty happy. Well. I was twelve
or thirteen then and I've smoked pot ever since. But for a different reason
now. ... When I was about sixteen I noticed one night I got high and my tics
weren't ticking. ... Since I smoked pot ... I could focus on school better.
My grades went up. The more pot I smoked, the better I could think, especially
since I had no pills in me. ... I don't want to go to prison for something
that truly helps my Tourette's syndrome and helps me function. I believe
and so does all my family that marihuana is the best medicine I have ever
had." claims anonymous patient from
"Tourette's
Syndrome".

Vaporization

2003: "Patients receiving physician approval to use cannabis should
be warned that chemicals released when the dried leaves and/or flowers are
burned put heavy smokers at increased risk for bronchitis and respiratory
infections. The risk can be avoided, however, by an alternative delivery
system: a device called a vaporizer that heats dried cannabis to a temperature
where cannabinoid vapors are released, but below the point of combustion,
where noxious and carcinogenic smoke toxins are formed. Patients can thus
inhale the pharmaceutically active cannabinoids without exposing themselves
to harmful respiratory toxins." claims
Dale Gieringer from
"Recommendation
to Patients: 'Dont smoke, Vaporize' ", O'Shaughnessy's Jouurnal
of the California Cannabis Research Medical Group, Summer 2003.

1993: "The current use of cigarette or pipe for the inhaling of
cannabinoids is recognized as delivering numerous irritants and possible
carcinogens along with the desired active principles to the tracheobronchial
tree and oral cavity. Vaporization separates out the more therapeutic chemical
components from the crude plant or resin impurities and breakdown products
of pyrrolysis." claims Tod Hiro
Mikuriya from
"Vaporization
of Cannabinoids: a Preferable Drug Delivery Route", Dec 16, 1993.

Weight

2013: "there are limited data regarding the relationship between cannabinoids
and metabolic processes. Epidemiologic studies have found lower prevalence rates of
obesity and diabetes mellitus in marijuana users compared with people who have never
used marijuana, suggesting a relationship between cannabinoids and peripheral metabolic processes."
claims Elizabeth A Penner, Hannah Buettner, Murray A Mittleman, from
"The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults".

2005: "Controlled studies have revealed therapeutic utility of
cannabinoids in the treatment of ... AIDS wasting syndrome ... THC itself
is approved in the U.S. by the FDA, and it is used in many other countries
for the prevention of vomiting during cancer chemotherapy, and for appetite
enhancement. We, and many others, have found that not only THC does that,
but also the endocannabinoids. This is one of the main reasons for high
endocannabinoid levels during hunger and so on. Now, THC can be used, and
is being used, for these two things. ... Sanofi-Synthélabo Recherché
in France is doing some interesting work. They have a compound, which is
an antagonist of the cannabinoid system, and they have tested it in about
eight thousand obese people. They have found that it is extremely useful.
Their appetite goes down slowly, as it should, and they lose weight. They
plan to introduce the compound in twelve months time, I think. They're doing
a lot of work in the field, and they expect huge sales." claims
Dr Raphael Mechoulam, as reported
by David Jay Brown,
"The
New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael
Mechoulam".

2000: "A study by researchers from the University of California, San
Francisco has found that patients with HIV infection taking protease inhibitors
do not experience short-term adverse virologic effects from using cannabinoids.
... All three groups gained weight. Part of that was due to regularly scheduled
meals and snacks being readily available. However, the placebo arm averaged
a gain of 1.30 kilograms while the subjects who took oral dronabinol gained
an average of 3.18 kilograms. Those who smoked marijuana gained an average
of 3.51 kilograms. Caloric intake reflected the same order." claims Dr
Donald I Abrams, Professor of Clinical
Medicine, University of California at San Francisco from
"Marijuana
Does Not Appear To Alter Viral Loads of HIV Patients Taking Protease
Inhibitors", July 13 2000.
also at
cannabismd.org/reports/abrams1.php,
marijuananews.com/news.php3?sid=253

1986: "I started feeling the changes pretty much right away. Smoking
marijuana also felt ten times better than taking Marinol
pill. It helped reduce my nausea and I could hold down
food better." claims Jim Kerns, cancer
patient whose weight fell from 220 to 140 pounds in his first year of
chemotherapy .

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ...
My neurologist prescribed the drugs Compazine and Antivert. They had little
affect on the nausea and no affect on the appetite, even after the dosage
was doubled. After a couple of weeks of feeling sick and not eating, I had
lost 15 pounds and no medication was helping. ... I decided to try smoking
Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke
were gone I began to relax and get an appetite. I could finally eat again.
Since that time, I have used cannabis to maintain a healthy body weight and
a decent standard of living. For years I left my prescription drugs setting
on the counter, as Cannabis was more effective." cliams John E Precup from
"Patient
Testimonials"

Withdrawal

2003: "The reportedly successful use of cannabis as an alternative
to alcohol, SSRI antidepressants, and stimulants (in
the treatment of ADHD) warrants serious, large-scale investigation. A necessary
first step is for the doctors who are monitoring patients using cannabis
for these purposes to agree on basic definitions, diagnostic criteria, etc.,
and to adopt uniform record-keeping methods. Hergenrathers observation
that half his cannabis-using patients have been able to stop taking
pharmaceutical drugs  and others have reduced their intake  suggests
a line of inquiry that belongs on a common interview form." claims
Fred Gardner from
"Which
Conditions are Californians Actually Treating With Cannabis?",
O'Shaughnessy's Jouurnal of the California Cannabis Research Medical
Group, Summer 2003.